Ignet

Gene Information

Gene symbol: ACE2

Gene name: angiotensin I converting enzyme (peptidyl-dipeptidase A) 2

HGNC ID: 13557

Related Genes

#	Gene Symbol	Number of hits
1	ACE	1 hits
2	ACTC1	1 hits
3	ADAM17	1 hits
4	AGT	1 hits
5	AGTR1	1 hits
6	AKT1	1 hits
7	ALB	1 hits
8	ANG	1 hits
9	APLN	1 hits
10	CD34	1 hits
11	COL1A1	1 hits
12	COL4A4	1 hits
13	DPP4	1 hits
14	HMOX1	1 hits
15	HNF1A	1 hits
16	HNF1B	1 hits
17	IL6	1 hits
18	INS	1 hits
19	MAS1	1 hits
20	MMEL1	1 hits
21	PPARGC1A	1 hits
22	REN	1 hits
23	RETN	1 hits
24	SPP1	1 hits
25	TLR4	1 hits
26	VEGFA	1 hits

Related Sentences

#	PMID	Sentence
1	12419208	The discovery of specific drugs that block either the key enzyme of the renin-angiotensin system, angiotensin-converting enzyme (ACE), or the receptor for its main effector angiotensin II, was a major step forward in the treatment of hypertension and heart failure.
2	12419208	Furthermore, a new ACE, angiotensin-converting enzyme 2 (ACE2), has been discovered which appears to negatively regulate the renin-angiotensin system.
3	12419208	We shall discuss the interplay of the various effector peptides generated by angiotensin-converting enzymes ACE and ACE2, highlighting the role of ACE2 as a negative regulator of the renin-angiotensin system.
4	12419208	The discovery of specific drugs that block either the key enzyme of the renin-angiotensin system, angiotensin-converting enzyme (ACE), or the receptor for its main effector angiotensin II, was a major step forward in the treatment of hypertension and heart failure.
5	12419208	Furthermore, a new ACE, angiotensin-converting enzyme 2 (ACE2), has been discovered which appears to negatively regulate the renin-angiotensin system.
6	12419208	We shall discuss the interplay of the various effector peptides generated by angiotensin-converting enzymes ACE and ACE2, highlighting the role of ACE2 as a negative regulator of the renin-angiotensin system.
7	12623933	ACE2, initially cloned from a human heart, is a recently described homologue of angiotensin-converting enzyme (ACE) but contains only a single enzymatic site that catalyzes the cleavage of angiotensin I to angiotensin 1-9 [Ang(1-9)] and is not inhibited by classic ACE inhibitors.
8	12623933	Although the role of ACE2 in the regulation of the renin-angiotensin system is not known, the renin-angiotensin system has been implicated in the pathogenesis of diabetic complications and in particular in diabetic nephropathy.
9	12623933	ACE2 and ACE gene and protein expression were measured in the kidney after 24 weeks of streptozocin diabetes.
10	12623933	ACE2 and ACE mRNA levels were decreased in diabetic renal tubules by approximately 50% and were not influenced by ACE inhibitor treatment with ramipril.
11	12623933	By immunostaining, both ACE2 and ACE protein were localized predominantly to renal tubules.
12	12623933	In the diabetic kidney, there was reduced ACE2 protein expression that was prevented by ACE inhibitor therapy.
13	12623933	ACE2, initially cloned from a human heart, is a recently described homologue of angiotensin-converting enzyme (ACE) but contains only a single enzymatic site that catalyzes the cleavage of angiotensin I to angiotensin 1-9 [Ang(1-9)] and is not inhibited by classic ACE inhibitors.
14	12623933	Although the role of ACE2 in the regulation of the renin-angiotensin system is not known, the renin-angiotensin system has been implicated in the pathogenesis of diabetic complications and in particular in diabetic nephropathy.
15	12623933	ACE2 and ACE gene and protein expression were measured in the kidney after 24 weeks of streptozocin diabetes.
16	12623933	ACE2 and ACE mRNA levels were decreased in diabetic renal tubules by approximately 50% and were not influenced by ACE inhibitor treatment with ramipril.
17	12623933	By immunostaining, both ACE2 and ACE protein were localized predominantly to renal tubules.
18	12623933	In the diabetic kidney, there was reduced ACE2 protein expression that was prevented by ACE inhibitor therapy.
19	12623933	ACE2, initially cloned from a human heart, is a recently described homologue of angiotensin-converting enzyme (ACE) but contains only a single enzymatic site that catalyzes the cleavage of angiotensin I to angiotensin 1-9 [Ang(1-9)] and is not inhibited by classic ACE inhibitors.
20	12623933	Although the role of ACE2 in the regulation of the renin-angiotensin system is not known, the renin-angiotensin system has been implicated in the pathogenesis of diabetic complications and in particular in diabetic nephropathy.
21	12623933	ACE2 and ACE gene and protein expression were measured in the kidney after 24 weeks of streptozocin diabetes.
22	12623933	ACE2 and ACE mRNA levels were decreased in diabetic renal tubules by approximately 50% and were not influenced by ACE inhibitor treatment with ramipril.
23	12623933	By immunostaining, both ACE2 and ACE protein were localized predominantly to renal tubules.
24	12623933	In the diabetic kidney, there was reduced ACE2 protein expression that was prevented by ACE inhibitor therapy.
25	12623933	ACE2, initially cloned from a human heart, is a recently described homologue of angiotensin-converting enzyme (ACE) but contains only a single enzymatic site that catalyzes the cleavage of angiotensin I to angiotensin 1-9 [Ang(1-9)] and is not inhibited by classic ACE inhibitors.
26	12623933	Although the role of ACE2 in the regulation of the renin-angiotensin system is not known, the renin-angiotensin system has been implicated in the pathogenesis of diabetic complications and in particular in diabetic nephropathy.
27	12623933	ACE2 and ACE gene and protein expression were measured in the kidney after 24 weeks of streptozocin diabetes.
28	12623933	ACE2 and ACE mRNA levels were decreased in diabetic renal tubules by approximately 50% and were not influenced by ACE inhibitor treatment with ramipril.
29	12623933	By immunostaining, both ACE2 and ACE protein were localized predominantly to renal tubules.
30	12623933	In the diabetic kidney, there was reduced ACE2 protein expression that was prevented by ACE inhibitor therapy.
31	12623933	ACE2, initially cloned from a human heart, is a recently described homologue of angiotensin-converting enzyme (ACE) but contains only a single enzymatic site that catalyzes the cleavage of angiotensin I to angiotensin 1-9 [Ang(1-9)] and is not inhibited by classic ACE inhibitors.
32	12623933	Although the role of ACE2 in the regulation of the renin-angiotensin system is not known, the renin-angiotensin system has been implicated in the pathogenesis of diabetic complications and in particular in diabetic nephropathy.
33	12623933	ACE2 and ACE gene and protein expression were measured in the kidney after 24 weeks of streptozocin diabetes.
34	12623933	ACE2 and ACE mRNA levels were decreased in diabetic renal tubules by approximately 50% and were not influenced by ACE inhibitor treatment with ramipril.
35	12623933	By immunostaining, both ACE2 and ACE protein were localized predominantly to renal tubules.
36	12623933	In the diabetic kidney, there was reduced ACE2 protein expression that was prevented by ACE inhibitor therapy.
37	12623933	ACE2, initially cloned from a human heart, is a recently described homologue of angiotensin-converting enzyme (ACE) but contains only a single enzymatic site that catalyzes the cleavage of angiotensin I to angiotensin 1-9 [Ang(1-9)] and is not inhibited by classic ACE inhibitors.
38	12623933	Although the role of ACE2 in the regulation of the renin-angiotensin system is not known, the renin-angiotensin system has been implicated in the pathogenesis of diabetic complications and in particular in diabetic nephropathy.
39	12623933	ACE2 and ACE gene and protein expression were measured in the kidney after 24 weeks of streptozocin diabetes.
40	12623933	ACE2 and ACE mRNA levels were decreased in diabetic renal tubules by approximately 50% and were not influenced by ACE inhibitor treatment with ramipril.
41	12623933	By immunostaining, both ACE2 and ACE protein were localized predominantly to renal tubules.
42	12623933	In the diabetic kidney, there was reduced ACE2 protein expression that was prevented by ACE inhibitor therapy.
43	15165741	The zinc metallopeptidase angiotensin-converting enzyme 2 (ACE2) is the only known human homologue of the key regulator of blood pressure angiotensin-converting enzyme (ACE).
44	15165741	Since its discovery in 2000, ACE2 has been implicated in heart function, hypertension and diabetes, with its effects being mediated, in part, through its ability to convert angiotensin II to angiotensin-(1-7).
45	15165741	The zinc metallopeptidase angiotensin-converting enzyme 2 (ACE2) is the only known human homologue of the key regulator of blood pressure angiotensin-converting enzyme (ACE).
46	15165741	Since its discovery in 2000, ACE2 has been implicated in heart function, hypertension and diabetes, with its effects being mediated, in part, through its ability to convert angiotensin II to angiotensin-(1-7).
47	15549171	Angiotensin-converting enzyme-2 (ACE2) is the first human homologue of ACE to be described.
48	15549171	ACE2 efficiently hydrolyses the potent vasoconstrictor angiotensin II to angiotensin (1-7).
49	15549171	It is a consequence of this action that ACE2 participates in the renin-angiotensin system.
50	15549171	However, ACE2 also hydrolyses dynorphin A (1-13), apelin-13 and des-Arg(9) bradykinin.
51	15549171	This paper reviews the biochemistry of ACE2 and discusses key findings such as the elucidation of crystal structures for ACE2 and testicular ACE and the development of ACE2 inhibitors that have now provided a basis for future research on this enzyme.
52	15549171	Angiotensin-converting enzyme-2 (ACE2) is the first human homologue of ACE to be described.
53	15549171	ACE2 efficiently hydrolyses the potent vasoconstrictor angiotensin II to angiotensin (1-7).
54	15549171	It is a consequence of this action that ACE2 participates in the renin-angiotensin system.
55	15549171	However, ACE2 also hydrolyses dynorphin A (1-13), apelin-13 and des-Arg(9) bradykinin.
56	15549171	This paper reviews the biochemistry of ACE2 and discusses key findings such as the elucidation of crystal structures for ACE2 and testicular ACE and the development of ACE2 inhibitors that have now provided a basis for future research on this enzyme.
57	15549171	Angiotensin-converting enzyme-2 (ACE2) is the first human homologue of ACE to be described.
58	15549171	ACE2 efficiently hydrolyses the potent vasoconstrictor angiotensin II to angiotensin (1-7).
59	15549171	It is a consequence of this action that ACE2 participates in the renin-angiotensin system.
60	15549171	However, ACE2 also hydrolyses dynorphin A (1-13), apelin-13 and des-Arg(9) bradykinin.
61	15549171	This paper reviews the biochemistry of ACE2 and discusses key findings such as the elucidation of crystal structures for ACE2 and testicular ACE and the development of ACE2 inhibitors that have now provided a basis for future research on this enzyme.
62	15549171	Angiotensin-converting enzyme-2 (ACE2) is the first human homologue of ACE to be described.
63	15549171	ACE2 efficiently hydrolyses the potent vasoconstrictor angiotensin II to angiotensin (1-7).
64	15549171	It is a consequence of this action that ACE2 participates in the renin-angiotensin system.
65	15549171	However, ACE2 also hydrolyses dynorphin A (1-13), apelin-13 and des-Arg(9) bradykinin.
66	15549171	This paper reviews the biochemistry of ACE2 and discusses key findings such as the elucidation of crystal structures for ACE2 and testicular ACE and the development of ACE2 inhibitors that have now provided a basis for future research on this enzyme.
67	15549171	Angiotensin-converting enzyme-2 (ACE2) is the first human homologue of ACE to be described.
68	15549171	ACE2 efficiently hydrolyses the potent vasoconstrictor angiotensin II to angiotensin (1-7).
69	15549171	It is a consequence of this action that ACE2 participates in the renin-angiotensin system.
70	15549171	However, ACE2 also hydrolyses dynorphin A (1-13), apelin-13 and des-Arg(9) bradykinin.
71	15549171	This paper reviews the biochemistry of ACE2 and discusses key findings such as the elucidation of crystal structures for ACE2 and testicular ACE and the development of ACE2 inhibitors that have now provided a basis for future research on this enzyme.
72	16297991	Identification of target genes of the transcription factor HNF1beta and HNF1alpha in a human embryonic kidney cell line.
73	16297991	By an identical approach, we identified that the related transcription factor HNF1alpha (TCF1) affects only nine genes in HEK293 cells and thus is a less efficient factor in these kidney cells.
74	16297991	The HNF1beta target genes dipeptidyl peptidase 4 (DPP4), angiotensin converting enzyme 2 (ACE2) and osteopontin (SPP1) are most likely direct target genes, as they contain functional HNF1 binding sites in their promoter region.
75	16781089	Angiotensin-converting enzyme 2 (ACE2), a newly identified member in the renin-angiotensin system (RAS), acts as a negative regulator of ACE.
76	16804085	ACE and ACE2 activity in diabetic mice.
77	16804085	ACE-related carboxypeptidase (ACE2) may counterbalance the angiotensin (ANG) II-promoting effects of ACE in tissues where both enzymes are found.
78	16804085	Alterations in renal ACE and ACE2 expression have been described in experimental models of diabetes, but ACE2 activity was not assessed in previous studies.
79	16804085	We developed a microplate-based fluorometric method for the concurrent determination of ACE and ACE2 activity in tissue samples.
80	16804085	Enzymatic activity (relative fluorescence unit [RFU] . microg protein(-1) . h(-1)) was examined in ACE and ACE2 knockout mice and in two rodent models of diabetes, the db/db and streptozotocin (STZ)-induced diabetic mice.
81	16804085	The availability of an assay for concurrent measurement of ACE and ACE2 activity should be helpful in the evaluation of kidney-specific alterations in the balance of these two carboxypeptidases, which are involved in the control of local ANG II formation and degradation.
82	16804085	ACE and ACE2 activity in diabetic mice.
83	16804085	ACE-related carboxypeptidase (ACE2) may counterbalance the angiotensin (ANG) II-promoting effects of ACE in tissues where both enzymes are found.
84	16804085	Alterations in renal ACE and ACE2 expression have been described in experimental models of diabetes, but ACE2 activity was not assessed in previous studies.
85	16804085	We developed a microplate-based fluorometric method for the concurrent determination of ACE and ACE2 activity in tissue samples.
86	16804085	Enzymatic activity (relative fluorescence unit [RFU] . microg protein(-1) . h(-1)) was examined in ACE and ACE2 knockout mice and in two rodent models of diabetes, the db/db and streptozotocin (STZ)-induced diabetic mice.
87	16804085	The availability of an assay for concurrent measurement of ACE and ACE2 activity should be helpful in the evaluation of kidney-specific alterations in the balance of these two carboxypeptidases, which are involved in the control of local ANG II formation and degradation.
88	16804085	ACE and ACE2 activity in diabetic mice.
89	16804085	ACE-related carboxypeptidase (ACE2) may counterbalance the angiotensin (ANG) II-promoting effects of ACE in tissues where both enzymes are found.
90	16804085	Alterations in renal ACE and ACE2 expression have been described in experimental models of diabetes, but ACE2 activity was not assessed in previous studies.
91	16804085	We developed a microplate-based fluorometric method for the concurrent determination of ACE and ACE2 activity in tissue samples.
92	16804085	Enzymatic activity (relative fluorescence unit [RFU] . microg protein(-1) . h(-1)) was examined in ACE and ACE2 knockout mice and in two rodent models of diabetes, the db/db and streptozotocin (STZ)-induced diabetic mice.
93	16804085	The availability of an assay for concurrent measurement of ACE and ACE2 activity should be helpful in the evaluation of kidney-specific alterations in the balance of these two carboxypeptidases, which are involved in the control of local ANG II formation and degradation.
94	16804085	ACE and ACE2 activity in diabetic mice.
95	16804085	ACE-related carboxypeptidase (ACE2) may counterbalance the angiotensin (ANG) II-promoting effects of ACE in tissues where both enzymes are found.
96	16804085	Alterations in renal ACE and ACE2 expression have been described in experimental models of diabetes, but ACE2 activity was not assessed in previous studies.
97	16804085	We developed a microplate-based fluorometric method for the concurrent determination of ACE and ACE2 activity in tissue samples.
98	16804085	Enzymatic activity (relative fluorescence unit [RFU] . microg protein(-1) . h(-1)) was examined in ACE and ACE2 knockout mice and in two rodent models of diabetes, the db/db and streptozotocin (STZ)-induced diabetic mice.
99	16804085	The availability of an assay for concurrent measurement of ACE and ACE2 activity should be helpful in the evaluation of kidney-specific alterations in the balance of these two carboxypeptidases, which are involved in the control of local ANG II formation and degradation.
100	16804085	ACE and ACE2 activity in diabetic mice.
101	16804085	ACE-related carboxypeptidase (ACE2) may counterbalance the angiotensin (ANG) II-promoting effects of ACE in tissues where both enzymes are found.
102	16804085	Alterations in renal ACE and ACE2 expression have been described in experimental models of diabetes, but ACE2 activity was not assessed in previous studies.
103	16804085	We developed a microplate-based fluorometric method for the concurrent determination of ACE and ACE2 activity in tissue samples.
104	16804085	Enzymatic activity (relative fluorescence unit [RFU] . microg protein(-1) . h(-1)) was examined in ACE and ACE2 knockout mice and in two rodent models of diabetes, the db/db and streptozotocin (STZ)-induced diabetic mice.
105	16804085	The availability of an assay for concurrent measurement of ACE and ACE2 activity should be helpful in the evaluation of kidney-specific alterations in the balance of these two carboxypeptidases, which are involved in the control of local ANG II formation and degradation.
106	16804085	ACE and ACE2 activity in diabetic mice.
107	16804085	ACE-related carboxypeptidase (ACE2) may counterbalance the angiotensin (ANG) II-promoting effects of ACE in tissues where both enzymes are found.
108	16804085	Alterations in renal ACE and ACE2 expression have been described in experimental models of diabetes, but ACE2 activity was not assessed in previous studies.
109	16804085	We developed a microplate-based fluorometric method for the concurrent determination of ACE and ACE2 activity in tissue samples.
110	16804085	Enzymatic activity (relative fluorescence unit [RFU] . microg protein(-1) . h(-1)) was examined in ACE and ACE2 knockout mice and in two rodent models of diabetes, the db/db and streptozotocin (STZ)-induced diabetic mice.
111	16804085	The availability of an assay for concurrent measurement of ACE and ACE2 activity should be helpful in the evaluation of kidney-specific alterations in the balance of these two carboxypeptidases, which are involved in the control of local ANG II formation and degradation.
112	17021266	Angiotensin-converting enzyme 2 (ACE2) expression has been shown to be altered in renal tubules from diabetic mice.
113	17021266	This study examined the localization of ACE and ACE2 within the glomerulus of kidneys from control (db/m) and diabetic (db/db) mice and the effect of chronic pharmacologic ACE2 inhibition.
114	17021266	For investigation of the significance of reduced glomerular ACE2 expression, db/db mice were treated for 16 wk with a specific ACE2 inhibitor (MLN-4760) alone or combined with telmisartan, a specific angiotensin II type 1 receptor blocker.
115	17021266	Urinary albumin excretion (UAE) increased significantly in MLN-4760-treated as compared with vehicle-treated db/db mice (743 +/- 200 versus 247 +/- 53.9 microg albumin/mg creatinine, respectively; P < 0.05), and the concomitant administration of telmisartan completely prevented the increase in UAE associated with the ACE2 inhibitor (161 +/- 56; P < 0.05).
116	17021266	It is concluded that ACE2 is localized in the podocyte and that in db/db mice glomerular expression of ACE2 is reduced whereas glomerular ACE expression is increased.
117	17021266	The finding that chronic ACE2 inhibition increases UAE suggests that ACE2, likely by modulating the levels of glomerular angiotensin II via its degradation, may be a target for therapeutic interventions that aim to reduce albuminuria and glomerular injury.
118	17021266	Angiotensin-converting enzyme 2 (ACE2) expression has been shown to be altered in renal tubules from diabetic mice.
119	17021266	This study examined the localization of ACE and ACE2 within the glomerulus of kidneys from control (db/m) and diabetic (db/db) mice and the effect of chronic pharmacologic ACE2 inhibition.
120	17021266	For investigation of the significance of reduced glomerular ACE2 expression, db/db mice were treated for 16 wk with a specific ACE2 inhibitor (MLN-4760) alone or combined with telmisartan, a specific angiotensin II type 1 receptor blocker.
121	17021266	Urinary albumin excretion (UAE) increased significantly in MLN-4760-treated as compared with vehicle-treated db/db mice (743 +/- 200 versus 247 +/- 53.9 microg albumin/mg creatinine, respectively; P < 0.05), and the concomitant administration of telmisartan completely prevented the increase in UAE associated with the ACE2 inhibitor (161 +/- 56; P < 0.05).
122	17021266	It is concluded that ACE2 is localized in the podocyte and that in db/db mice glomerular expression of ACE2 is reduced whereas glomerular ACE expression is increased.
123	17021266	The finding that chronic ACE2 inhibition increases UAE suggests that ACE2, likely by modulating the levels of glomerular angiotensin II via its degradation, may be a target for therapeutic interventions that aim to reduce albuminuria and glomerular injury.
124	17021266	Angiotensin-converting enzyme 2 (ACE2) expression has been shown to be altered in renal tubules from diabetic mice.
125	17021266	This study examined the localization of ACE and ACE2 within the glomerulus of kidneys from control (db/m) and diabetic (db/db) mice and the effect of chronic pharmacologic ACE2 inhibition.
126	17021266	For investigation of the significance of reduced glomerular ACE2 expression, db/db mice were treated for 16 wk with a specific ACE2 inhibitor (MLN-4760) alone or combined with telmisartan, a specific angiotensin II type 1 receptor blocker.
127	17021266	Urinary albumin excretion (UAE) increased significantly in MLN-4760-treated as compared with vehicle-treated db/db mice (743 +/- 200 versus 247 +/- 53.9 microg albumin/mg creatinine, respectively; P < 0.05), and the concomitant administration of telmisartan completely prevented the increase in UAE associated with the ACE2 inhibitor (161 +/- 56; P < 0.05).
128	17021266	It is concluded that ACE2 is localized in the podocyte and that in db/db mice glomerular expression of ACE2 is reduced whereas glomerular ACE expression is increased.
129	17021266	The finding that chronic ACE2 inhibition increases UAE suggests that ACE2, likely by modulating the levels of glomerular angiotensin II via its degradation, may be a target for therapeutic interventions that aim to reduce albuminuria and glomerular injury.
130	17021266	Angiotensin-converting enzyme 2 (ACE2) expression has been shown to be altered in renal tubules from diabetic mice.
131	17021266	This study examined the localization of ACE and ACE2 within the glomerulus of kidneys from control (db/m) and diabetic (db/db) mice and the effect of chronic pharmacologic ACE2 inhibition.
132	17021266	For investigation of the significance of reduced glomerular ACE2 expression, db/db mice were treated for 16 wk with a specific ACE2 inhibitor (MLN-4760) alone or combined with telmisartan, a specific angiotensin II type 1 receptor blocker.
133	17021266	Urinary albumin excretion (UAE) increased significantly in MLN-4760-treated as compared with vehicle-treated db/db mice (743 +/- 200 versus 247 +/- 53.9 microg albumin/mg creatinine, respectively; P < 0.05), and the concomitant administration of telmisartan completely prevented the increase in UAE associated with the ACE2 inhibitor (161 +/- 56; P < 0.05).
134	17021266	It is concluded that ACE2 is localized in the podocyte and that in db/db mice glomerular expression of ACE2 is reduced whereas glomerular ACE expression is increased.
135	17021266	The finding that chronic ACE2 inhibition increases UAE suggests that ACE2, likely by modulating the levels of glomerular angiotensin II via its degradation, may be a target for therapeutic interventions that aim to reduce albuminuria and glomerular injury.
136	17021266	Angiotensin-converting enzyme 2 (ACE2) expression has been shown to be altered in renal tubules from diabetic mice.
137	17021266	This study examined the localization of ACE and ACE2 within the glomerulus of kidneys from control (db/m) and diabetic (db/db) mice and the effect of chronic pharmacologic ACE2 inhibition.
138	17021266	For investigation of the significance of reduced glomerular ACE2 expression, db/db mice were treated for 16 wk with a specific ACE2 inhibitor (MLN-4760) alone or combined with telmisartan, a specific angiotensin II type 1 receptor blocker.
139	17021266	Urinary albumin excretion (UAE) increased significantly in MLN-4760-treated as compared with vehicle-treated db/db mice (743 +/- 200 versus 247 +/- 53.9 microg albumin/mg creatinine, respectively; P < 0.05), and the concomitant administration of telmisartan completely prevented the increase in UAE associated with the ACE2 inhibitor (161 +/- 56; P < 0.05).
140	17021266	It is concluded that ACE2 is localized in the podocyte and that in db/db mice glomerular expression of ACE2 is reduced whereas glomerular ACE expression is increased.
141	17021266	The finding that chronic ACE2 inhibition increases UAE suggests that ACE2, likely by modulating the levels of glomerular angiotensin II via its degradation, may be a target for therapeutic interventions that aim to reduce albuminuria and glomerular injury.
142	17021266	Angiotensin-converting enzyme 2 (ACE2) expression has been shown to be altered in renal tubules from diabetic mice.
143	17021266	This study examined the localization of ACE and ACE2 within the glomerulus of kidneys from control (db/m) and diabetic (db/db) mice and the effect of chronic pharmacologic ACE2 inhibition.
144	17021266	For investigation of the significance of reduced glomerular ACE2 expression, db/db mice were treated for 16 wk with a specific ACE2 inhibitor (MLN-4760) alone or combined with telmisartan, a specific angiotensin II type 1 receptor blocker.
145	17021266	Urinary albumin excretion (UAE) increased significantly in MLN-4760-treated as compared with vehicle-treated db/db mice (743 +/- 200 versus 247 +/- 53.9 microg albumin/mg creatinine, respectively; P < 0.05), and the concomitant administration of telmisartan completely prevented the increase in UAE associated with the ACE2 inhibitor (161 +/- 56; P < 0.05).
146	17021266	It is concluded that ACE2 is localized in the podocyte and that in db/db mice glomerular expression of ACE2 is reduced whereas glomerular ACE expression is increased.
147	17021266	The finding that chronic ACE2 inhibition increases UAE suggests that ACE2, likely by modulating the levels of glomerular angiotensin II via its degradation, may be a target for therapeutic interventions that aim to reduce albuminuria and glomerular injury.
148	17464936	In particular, the human homologue of ACE (ACE2) has added a higher level of complexity to the RAAS.
149	17579661	ACE2 inhibition worsens glomerular injury in association with increased ACE expression in streptozotocin-induced diabetic mice.
150	17579661	Angiotensin converting enzyme 2 (ACE2) is localized to the glomerular epithelial cells.
151	17579661	Since ACE2 promotes the degradation of angiotensin II, a decrease in ACE2 activity could lead to the development of glomerular injury.
152	17579661	In renal vessels, ACE expression was also increased in the diabetic mice and, again, further increased in those diabetic mice treated with the ACE2 inhibitor.
153	17579661	Our study shows that chronic pharmacologic ACE2 inhibition worsens glomerular injury in streptozotocin-induced diabetic mice in association with increased ACE expression.
154	17579661	ACE2 inhibition worsens glomerular injury in association with increased ACE expression in streptozotocin-induced diabetic mice.
155	17579661	Angiotensin converting enzyme 2 (ACE2) is localized to the glomerular epithelial cells.
156	17579661	Since ACE2 promotes the degradation of angiotensin II, a decrease in ACE2 activity could lead to the development of glomerular injury.
157	17579661	In renal vessels, ACE expression was also increased in the diabetic mice and, again, further increased in those diabetic mice treated with the ACE2 inhibitor.
158	17579661	Our study shows that chronic pharmacologic ACE2 inhibition worsens glomerular injury in streptozotocin-induced diabetic mice in association with increased ACE expression.
159	17579661	ACE2 inhibition worsens glomerular injury in association with increased ACE expression in streptozotocin-induced diabetic mice.
160	17579661	Angiotensin converting enzyme 2 (ACE2) is localized to the glomerular epithelial cells.
161	17579661	Since ACE2 promotes the degradation of angiotensin II, a decrease in ACE2 activity could lead to the development of glomerular injury.
162	17579661	In renal vessels, ACE expression was also increased in the diabetic mice and, again, further increased in those diabetic mice treated with the ACE2 inhibitor.
163	17579661	Our study shows that chronic pharmacologic ACE2 inhibition worsens glomerular injury in streptozotocin-induced diabetic mice in association with increased ACE expression.
164	17579661	ACE2 inhibition worsens glomerular injury in association with increased ACE expression in streptozotocin-induced diabetic mice.
165	17579661	Angiotensin converting enzyme 2 (ACE2) is localized to the glomerular epithelial cells.
166	17579661	Since ACE2 promotes the degradation of angiotensin II, a decrease in ACE2 activity could lead to the development of glomerular injury.
167	17579661	In renal vessels, ACE expression was also increased in the diabetic mice and, again, further increased in those diabetic mice treated with the ACE2 inhibitor.
168	17579661	Our study shows that chronic pharmacologic ACE2 inhibition worsens glomerular injury in streptozotocin-induced diabetic mice in association with increased ACE expression.
169	17579661	ACE2 inhibition worsens glomerular injury in association with increased ACE expression in streptozotocin-induced diabetic mice.
170	17579661	Angiotensin converting enzyme 2 (ACE2) is localized to the glomerular epithelial cells.
171	17579661	Since ACE2 promotes the degradation of angiotensin II, a decrease in ACE2 activity could lead to the development of glomerular injury.
172	17579661	In renal vessels, ACE expression was also increased in the diabetic mice and, again, further increased in those diabetic mice treated with the ACE2 inhibitor.
173	17579661	Our study shows that chronic pharmacologic ACE2 inhibition worsens glomerular injury in streptozotocin-induced diabetic mice in association with increased ACE expression.
174	17600118	Loss of angiotensin-converting enzyme-2 (Ace2) accelerates diabetic kidney injury.
175	17600118	Ace2(-/y) Ins2(WT/C96Y) mice exhibited a twofold increase in the urinary albumin excretion rate compared with Ace2(+/y)Ins2(WT/C96Y) mice despite similar blood glucose levels.
176	17600118	Ace2(-/y)Ins2(WT/C96Y) mice were the only group to exhibit increased mesangial matrix scores and glomerular basement membrane thicknesses compared with Ace2(+/y)Ins2(WT/WT) mice, accompanied by increased fibronectin and alpha-smooth muscle actin immunostaining in the glomeruli of Ace2(-/y) Ins2(WT/C96Y) mice.
177	17600118	Although kidney levels of angiotensin (Ang) II were not increased in the diabetic mice, treatment with an Ang II receptor blocker reduced urinary albumin excretion rate in Ace2(-/y)Ins2(WT/C96Y) mice, suggesting that acceleration of kidney injury in these mice is Ang II-mediated.
178	17600118	Loss of angiotensin-converting enzyme-2 (Ace2) accelerates diabetic kidney injury.
179	17600118	Ace2(-/y) Ins2(WT/C96Y) mice exhibited a twofold increase in the urinary albumin excretion rate compared with Ace2(+/y)Ins2(WT/C96Y) mice despite similar blood glucose levels.
180	17600118	Ace2(-/y)Ins2(WT/C96Y) mice were the only group to exhibit increased mesangial matrix scores and glomerular basement membrane thicknesses compared with Ace2(+/y)Ins2(WT/WT) mice, accompanied by increased fibronectin and alpha-smooth muscle actin immunostaining in the glomeruli of Ace2(-/y) Ins2(WT/C96Y) mice.
181	17600118	Although kidney levels of angiotensin (Ang) II were not increased in the diabetic mice, treatment with an Ang II receptor blocker reduced urinary albumin excretion rate in Ace2(-/y)Ins2(WT/C96Y) mice, suggesting that acceleration of kidney injury in these mice is Ang II-mediated.
182	17600118	Loss of angiotensin-converting enzyme-2 (Ace2) accelerates diabetic kidney injury.
183	17600118	Ace2(-/y) Ins2(WT/C96Y) mice exhibited a twofold increase in the urinary albumin excretion rate compared with Ace2(+/y)Ins2(WT/C96Y) mice despite similar blood glucose levels.
184	17600118	Ace2(-/y)Ins2(WT/C96Y) mice were the only group to exhibit increased mesangial matrix scores and glomerular basement membrane thicknesses compared with Ace2(+/y)Ins2(WT/WT) mice, accompanied by increased fibronectin and alpha-smooth muscle actin immunostaining in the glomeruli of Ace2(-/y) Ins2(WT/C96Y) mice.
185	17600118	Although kidney levels of angiotensin (Ang) II were not increased in the diabetic mice, treatment with an Ang II receptor blocker reduced urinary albumin excretion rate in Ace2(-/y)Ins2(WT/C96Y) mice, suggesting that acceleration of kidney injury in these mice is Ang II-mediated.
186	17600118	Loss of angiotensin-converting enzyme-2 (Ace2) accelerates diabetic kidney injury.
187	17600118	Ace2(-/y) Ins2(WT/C96Y) mice exhibited a twofold increase in the urinary albumin excretion rate compared with Ace2(+/y)Ins2(WT/C96Y) mice despite similar blood glucose levels.
188	17600118	Ace2(-/y)Ins2(WT/C96Y) mice were the only group to exhibit increased mesangial matrix scores and glomerular basement membrane thicknesses compared with Ace2(+/y)Ins2(WT/WT) mice, accompanied by increased fibronectin and alpha-smooth muscle actin immunostaining in the glomeruli of Ace2(-/y) Ins2(WT/C96Y) mice.
189	17600118	Although kidney levels of angiotensin (Ang) II were not increased in the diabetic mice, treatment with an Ang II receptor blocker reduced urinary albumin excretion rate in Ace2(-/y)Ins2(WT/C96Y) mice, suggesting that acceleration of kidney injury in these mice is Ang II-mediated.
190	17897017	Angiotensin converting enzyme (ACE) is a key enzyme in the renin angiotensin system (RAS) and converts angiotensin (Ang) I to the vasoconstrictor Ang II, which is thought to be responsible for most of the physiological and pathophysiological effects of the RAS.
191	17897017	This classical view of the RAS was challenged with the discovery of the enzyme, ACE2 which both degrades Ang II and leads to formation of the vasodilatory and anti-proliferative peptide, Ang 1-7.
192	17897017	It is believed that ACE2 acts in a counter-regulatory manner to ACE to modulate the balance between vasoconstrictors and vasodilators within the heart and kidney, and may thus play a significant role in the pathophysiology of cardiac and renal disease.
193	17897017	Angiotensin converting enzyme (ACE) is a key enzyme in the renin angiotensin system (RAS) and converts angiotensin (Ang) I to the vasoconstrictor Ang II, which is thought to be responsible for most of the physiological and pathophysiological effects of the RAS.
194	17897017	This classical view of the RAS was challenged with the discovery of the enzyme, ACE2 which both degrades Ang II and leads to formation of the vasodilatory and anti-proliferative peptide, Ang 1-7.
195	17897017	It is believed that ACE2 acts in a counter-regulatory manner to ACE to modulate the balance between vasoconstrictors and vasodilators within the heart and kidney, and may thus play a significant role in the pathophysiology of cardiac and renal disease.
196	18223023	Angiotensin-converting enzyme (ACE) 2 is a homologue of ACE with enzymatic activity that seems to counterbalance the angiotensin II-promoting effect of ACE.
197	18223023	While ACE promotes angiotensin (Ang) II formation from Ang I, ACE2 degrades Ang II and Ang I.
198	18223023	Taken together, these findings suggest that a decrease in ACE2 may be involved in diabetic kidney disease, possibly by disrupting the metabolism of angiotensin peptides in such a way that angiotensin II degradation within the glomerulus may be diminished.
199	18223023	Angiotensin-converting enzyme (ACE) 2 is a homologue of ACE with enzymatic activity that seems to counterbalance the angiotensin II-promoting effect of ACE.
200	18223023	While ACE promotes angiotensin (Ang) II formation from Ang I, ACE2 degrades Ang II and Ang I.
201	18223023	Taken together, these findings suggest that a decrease in ACE2 may be involved in diabetic kidney disease, possibly by disrupting the metabolism of angiotensin peptides in such a way that angiotensin II degradation within the glomerulus may be diminished.
202	18235039	ACE2 deficiency modifies renoprotection afforded by ACE inhibition in experimental diabetes.
203	18307733	Angiotensin converting enzyme 2 (ACE2) is an important homeostatic component of the renin angiotensin system (RAS).
204	18307733	ACE2 both degrades the vasoconstrictor, angiotensin II and generates the potent vasodilator peptide, angiotensin 1-7.
205	18307733	ACE2 is highly expressed in the healthy kidney, particularly in the proximal tubules, where it colocalizes with ACE and angiotensin receptors. 3.
206	18307733	Kidney disease and subtotal nephrectomy is associated with a reduction in renal ACE2 expression, possibly facilitating the damaging effects of angiotensin II in the failing kidney.
207	18307733	Angiotensin converting enzyme 2 (ACE2) is an important homeostatic component of the renin angiotensin system (RAS).
208	18307733	ACE2 both degrades the vasoconstrictor, angiotensin II and generates the potent vasodilator peptide, angiotensin 1-7.
209	18307733	ACE2 is highly expressed in the healthy kidney, particularly in the proximal tubules, where it colocalizes with ACE and angiotensin receptors. 3.
210	18307733	Kidney disease and subtotal nephrectomy is associated with a reduction in renal ACE2 expression, possibly facilitating the damaging effects of angiotensin II in the failing kidney.
211	18307733	Angiotensin converting enzyme 2 (ACE2) is an important homeostatic component of the renin angiotensin system (RAS).
212	18307733	ACE2 both degrades the vasoconstrictor, angiotensin II and generates the potent vasodilator peptide, angiotensin 1-7.
213	18307733	ACE2 is highly expressed in the healthy kidney, particularly in the proximal tubules, where it colocalizes with ACE and angiotensin receptors. 3.
214	18307733	Kidney disease and subtotal nephrectomy is associated with a reduction in renal ACE2 expression, possibly facilitating the damaging effects of angiotensin II in the failing kidney.
215	18307733	Angiotensin converting enzyme 2 (ACE2) is an important homeostatic component of the renin angiotensin system (RAS).
216	18307733	ACE2 both degrades the vasoconstrictor, angiotensin II and generates the potent vasodilator peptide, angiotensin 1-7.
217	18307733	ACE2 is highly expressed in the healthy kidney, particularly in the proximal tubules, where it colocalizes with ACE and angiotensin receptors. 3.
218	18307733	Kidney disease and subtotal nephrectomy is associated with a reduction in renal ACE2 expression, possibly facilitating the damaging effects of angiotensin II in the failing kidney.
219	18355768	Angiotensinogen (AGT), angiotensin II (Ang II), angiotensin converting enzyme (ACE), and angiotensin converting enzyme 2 (ACE2) were measured in glomeruli isolated from 4-week-old STZ-diabetic rats and 32-week-old ZDF rats.
220	18355768	Glomerular AGT and Ang II levels were increased significantly in STZ-diabetic compared with nondiabetic control rats, accompanied by a reduction in ACE2 activity.
221	18355768	In contrast, glomerular AGT, Ang II, and ACE2 were similar in ZDF rats and lean controls.
222	18355768	Angiotensinogen (AGT), angiotensin II (Ang II), angiotensin converting enzyme (ACE), and angiotensin converting enzyme 2 (ACE2) were measured in glomeruli isolated from 4-week-old STZ-diabetic rats and 32-week-old ZDF rats.
223	18355768	Glomerular AGT and Ang II levels were increased significantly in STZ-diabetic compared with nondiabetic control rats, accompanied by a reduction in ACE2 activity.
224	18355768	In contrast, glomerular AGT, Ang II, and ACE2 were similar in ZDF rats and lean controls.
225	18355768	Angiotensinogen (AGT), angiotensin II (Ang II), angiotensin converting enzyme (ACE), and angiotensin converting enzyme 2 (ACE2) were measured in glomeruli isolated from 4-week-old STZ-diabetic rats and 32-week-old ZDF rats.
226	18355768	Glomerular AGT and Ang II levels were increased significantly in STZ-diabetic compared with nondiabetic control rats, accompanied by a reduction in ACE2 activity.
227	18355768	In contrast, glomerular AGT, Ang II, and ACE2 were similar in ZDF rats and lean controls.
228	18371537	Expression of ACE and ACE2 in individuals with diabetic kidney disease and healthy controls.
229	18372234	Concurrently, we found in D and DS an increase in cardiac beta-myosin heavy chain, atrial natriuretic peptide, skeletal alpha-actin mRNA, type III collagen, and transforming growth factor-beta.
230	18372234	Myocardial angiotensin-converting enzyme (ACE) mRNA levels were increased while ACE2 mRNA levels were decreased in both D and DS groups.
231	18372234	Cardiac angiotensin-1 (AT1) receptor protein levels were unchanged but the levels of phosphorylated (p) ERK and Jun-NH(2)-protein kinase (JNK) were increased in D and DS.
232	18372234	The increase in ACE, the decrease in ACE2, and the increase in cardiac pERK and pJNK suggest an increase in free angiotensin II and AT1R signaling in the diabetic myocardium as a possible mechanism contributing to cardiac remodeling in diabetes.
233	18372234	Concurrently, we found in D and DS an increase in cardiac beta-myosin heavy chain, atrial natriuretic peptide, skeletal alpha-actin mRNA, type III collagen, and transforming growth factor-beta.
234	18372234	Myocardial angiotensin-converting enzyme (ACE) mRNA levels were increased while ACE2 mRNA levels were decreased in both D and DS groups.
235	18372234	Cardiac angiotensin-1 (AT1) receptor protein levels were unchanged but the levels of phosphorylated (p) ERK and Jun-NH(2)-protein kinase (JNK) were increased in D and DS.
236	18372234	The increase in ACE, the decrease in ACE2, and the increase in cardiac pERK and pJNK suggest an increase in free angiotensin II and AT1R signaling in the diabetic myocardium as a possible mechanism contributing to cardiac remodeling in diabetes.
237	18389211	Urinary mRNA expression of ACE and ACE2 in human type 2 diabetic nephropathy.
238	18679036	Renal ACE and ACE2 expression in early diabetic rats.
239	18948167	In this review we will examine the role of the renin-angiotensin system in the physiopathology and treatment of diabetes and highlight the potential benefits of the ACE2/Ang-(1-7)/Mas receptor axis, focusing on recent data about ACE2.
240	18956256	This study aimed to investigate the role of angiotensin-converting enzyme 2 (ACE2) in regulating glucose homeostasis.
241	18956256	Glucose tolerance test, insulin secretion test, and insulin tolerance test were performed in age-matched male ACE2 knockout (KO) and wild-type (WT) mice.
242	18956256	Male ACE2 KO mice displayed a selective decrease in first-phase insulin secretion in response to glucose and a progressive impairment of glucose tolerance compared with age- and sex-matched WT mice.
243	18956256	On the other hand, insulin sensitivity of the peripheral tissue in age-matched ACE2 KO and WT mice showed no difference.
244	18956256	This study aimed to investigate the role of angiotensin-converting enzyme 2 (ACE2) in regulating glucose homeostasis.
245	18956256	Glucose tolerance test, insulin secretion test, and insulin tolerance test were performed in age-matched male ACE2 knockout (KO) and wild-type (WT) mice.
246	18956256	Male ACE2 KO mice displayed a selective decrease in first-phase insulin secretion in response to glucose and a progressive impairment of glucose tolerance compared with age- and sex-matched WT mice.
247	18956256	On the other hand, insulin sensitivity of the peripheral tissue in age-matched ACE2 KO and WT mice showed no difference.
248	18956256	This study aimed to investigate the role of angiotensin-converting enzyme 2 (ACE2) in regulating glucose homeostasis.
249	18956256	Glucose tolerance test, insulin secretion test, and insulin tolerance test were performed in age-matched male ACE2 knockout (KO) and wild-type (WT) mice.
250	18956256	Male ACE2 KO mice displayed a selective decrease in first-phase insulin secretion in response to glucose and a progressive impairment of glucose tolerance compared with age- and sex-matched WT mice.
251	18956256	On the other hand, insulin sensitivity of the peripheral tissue in age-matched ACE2 KO and WT mice showed no difference.
252	18956256	This study aimed to investigate the role of angiotensin-converting enzyme 2 (ACE2) in regulating glucose homeostasis.
253	18956256	Glucose tolerance test, insulin secretion test, and insulin tolerance test were performed in age-matched male ACE2 knockout (KO) and wild-type (WT) mice.
254	18956256	Male ACE2 KO mice displayed a selective decrease in first-phase insulin secretion in response to glucose and a progressive impairment of glucose tolerance compared with age- and sex-matched WT mice.
255	18956256	On the other hand, insulin sensitivity of the peripheral tissue in age-matched ACE2 KO and WT mice showed no difference.
256	19034303	Angiotensin converting enzyme (ACE) generates angiotensin II from angiotensin I, which plays a critical role in the pathophysiology of diabetic nephropathy.
257	19034303	However, ACE2 generates angiotensin 1-7, which may protect the kidney by attenuating the effects of angiotensin II, since deletion of the Ace2 gene leads to glomerulosclerosis in mice, and pharmacologic inhibition of ACE2 exacerbates experimental diabetic nephropathy.
258	19034303	We measured ACE2 and ACE expression in renal biopsies of patients with kidney disease due to type 2 diabetes to determine if the expression pattern is specific to diabetic nephropathy.
259	19034303	ACE2 and ACE mRNA levels were measured by real-time PCR in laser microdissected renal biopsies from 13 diabetic and 8 control patients.
260	19034303	ACE2 mRNA was significantly reduced by more than half in both the glomeruli and proximal tubules of the diabetic patients compared to controls, but ACE mRNA was increased in both compartments.
261	19034303	Angiotensin converting enzyme (ACE) generates angiotensin II from angiotensin I, which plays a critical role in the pathophysiology of diabetic nephropathy.
262	19034303	However, ACE2 generates angiotensin 1-7, which may protect the kidney by attenuating the effects of angiotensin II, since deletion of the Ace2 gene leads to glomerulosclerosis in mice, and pharmacologic inhibition of ACE2 exacerbates experimental diabetic nephropathy.
263	19034303	We measured ACE2 and ACE expression in renal biopsies of patients with kidney disease due to type 2 diabetes to determine if the expression pattern is specific to diabetic nephropathy.
264	19034303	ACE2 and ACE mRNA levels were measured by real-time PCR in laser microdissected renal biopsies from 13 diabetic and 8 control patients.
265	19034303	ACE2 mRNA was significantly reduced by more than half in both the glomeruli and proximal tubules of the diabetic patients compared to controls, but ACE mRNA was increased in both compartments.
266	19034303	Angiotensin converting enzyme (ACE) generates angiotensin II from angiotensin I, which plays a critical role in the pathophysiology of diabetic nephropathy.
267	19034303	However, ACE2 generates angiotensin 1-7, which may protect the kidney by attenuating the effects of angiotensin II, since deletion of the Ace2 gene leads to glomerulosclerosis in mice, and pharmacologic inhibition of ACE2 exacerbates experimental diabetic nephropathy.
268	19034303	We measured ACE2 and ACE expression in renal biopsies of patients with kidney disease due to type 2 diabetes to determine if the expression pattern is specific to diabetic nephropathy.
269	19034303	ACE2 and ACE mRNA levels were measured by real-time PCR in laser microdissected renal biopsies from 13 diabetic and 8 control patients.
270	19034303	ACE2 mRNA was significantly reduced by more than half in both the glomeruli and proximal tubules of the diabetic patients compared to controls, but ACE mRNA was increased in both compartments.
271	19034303	Angiotensin converting enzyme (ACE) generates angiotensin II from angiotensin I, which plays a critical role in the pathophysiology of diabetic nephropathy.
272	19034303	However, ACE2 generates angiotensin 1-7, which may protect the kidney by attenuating the effects of angiotensin II, since deletion of the Ace2 gene leads to glomerulosclerosis in mice, and pharmacologic inhibition of ACE2 exacerbates experimental diabetic nephropathy.
273	19034303	We measured ACE2 and ACE expression in renal biopsies of patients with kidney disease due to type 2 diabetes to determine if the expression pattern is specific to diabetic nephropathy.
274	19034303	ACE2 and ACE mRNA levels were measured by real-time PCR in laser microdissected renal biopsies from 13 diabetic and 8 control patients.
275	19034303	ACE2 mRNA was significantly reduced by more than half in both the glomeruli and proximal tubules of the diabetic patients compared to controls, but ACE mRNA was increased in both compartments.
276	19065996	The identification of the renin/prorenin receptor, the angiotensin-converting enzyme homologue ACE2 as an angiotensin peptide processing enzyme, Mas as a receptor for Ang-(1-7) and the possibility of signaling through ACE, have contributed to switch our understanding of the RAS from the classical limited-proteolysis linear cascade to a cascade with multiple mediators, multiple receptors, and multi-functional enzymes.
277	19333547	This study was to determine whether the damage was correlated with expression of the SARS coronavirus receptor, angiotensin converting enzyme 2 (ACE2), in different organs, especially in the endocrine tissues of the pancreas, and to elucidate the pathogenesis of glucose intolerance in SARS patients.
278	19404293	Angiotensin-converting enzyme 2 (ACE2) gene and protein expression in diabetic patients without nephropathy.
279	19846569	Major role for ACE-independent intrarenal ANG II formation in type II diabetes.
280	19846569	Combination therapy of angiotensin-converting enzyme (ACE) inhibition and AT(1) receptor blockade has been shown to provide greater renoprotection than ACE inhibitor alone in human diabetic nephropathy, suggesting that ACE-independent pathways for ANG II formation are of major significance in disease progression.
281	19846569	Studies were performed to determine the magnitude of intrarenal ACE-independent formation of ANG II in type II diabetes.
282	19846569	Although renal cortical ACE protein activity [2.1 +/- 0.8 vs. 9.2 +/- 2.1 arbitrary fluorescence units (AFU) x mg(-1) x min(-1)] and intensity of immunohistochemical staining were significantly reduced and ACE2 protein activity (16.7 +/- 3.2 vs. 7.2 +/- 2.4 AFU x mg(-1) x min(-1)) and intensity elevated, kidney ANG I (113 +/- 24 vs. 110 +/- 45 fmol/g) and ANG II (1,017 +/- 165 vs. 788 +/- 99 fmol/g) levels were not different between diabetic and control mice.
283	19846569	Afferent arteriole vasoconstriction due to conversion of ANG I to ANG II was similar in magnitude in kidneys of diabetic (-28 +/- 3% at 1 microM) and control (-23 +/- 3% at 1 microM) mice; a response completely inhibited by AT(1) receptor blockade.
284	19846569	In control kidneys, afferent arteriole vasoconstriction produced by ANG I was significantly attenuated by ACE inhibition, but not by serine protease inhibition.
285	19846569	In contrast, afferent arteriole vasoconstriction produced by intrarenal conversion of ANG I to ANG II was significantly attenuated by serine protease inhibition, but not by ACE inhibition in diabetic kidneys.
286	19846569	In conclusion, there is a switch from ACE-dependent to serine protease-dependent ANG II formation in the type II diabetic kidney.
287	20186149	As angiotensin-converting enzyme-2 (ACE2) was identified as a negative regulator of the renin-angiotensin system, there have been many reports concerning its role in several tissues, including the kidney.
288	20186149	Periodic acid-Schiff-stained cross-section of diabetic ACE2-KO mice showed a more severe time-dependent increase in glomerular/tubulointerstitial damage than did that of wild-type mice, confirmed by the immunostaining of alpha-smooth muscle actin, collagen IV and F4-80 antigen.
289	20186149	Glomeruli of diabetic ACE2-KO mice showed earlier and more severe decrease in the expression of nephrin, whose degradation is involved in the onset of albuminuria, and more potent increase of vascular endothelial growth factor expression.
290	20186149	The renal-protective effect of ACE2 might involve more than just suppressing angiotensin II-mediated AT1 receptor signaling.
291	20186149	As angiotensin-converting enzyme-2 (ACE2) was identified as a negative regulator of the renin-angiotensin system, there have been many reports concerning its role in several tissues, including the kidney.
292	20186149	Periodic acid-Schiff-stained cross-section of diabetic ACE2-KO mice showed a more severe time-dependent increase in glomerular/tubulointerstitial damage than did that of wild-type mice, confirmed by the immunostaining of alpha-smooth muscle actin, collagen IV and F4-80 antigen.
293	20186149	Glomeruli of diabetic ACE2-KO mice showed earlier and more severe decrease in the expression of nephrin, whose degradation is involved in the onset of albuminuria, and more potent increase of vascular endothelial growth factor expression.
294	20186149	The renal-protective effect of ACE2 might involve more than just suppressing angiotensin II-mediated AT1 receptor signaling.
295	20422227	Increased accumulation of extracellular matrix proteins in the glomeruli and marked upregulation of angiotensinogen, angiotensin II type 1 receptor, angiotensin-converting enzyme, transforming growth factor beta-1 (TGF-beta1), and plasminogen activator inhibitor-1 (PAI-1) gene expression were evident in the renal cortex of hypertensive offspring of diabetic mothers.
296	20422227	By contrast, angiotensin-converting enzyme-2 (ACE2) gene expression was lower in the hypertensive offspring of diabetic mothers than in that of non-diabetic mothers.
297	20422227	These data indicate that maternal diabetes induces perinatal programming of hypertension, renal injury, and glucose intolerance in the offspring and suggest a central role for the activation of the intrarenal renin-angiotensin system and TGF-beta1 gene expression in this process.
298	20660625	Angiotensin I-converting enzyme type 2 (ACE2) gene therapy improves glycemic control in diabetic mice.
299	20844835	The reduced expression of angiotensin-converting enzyme (ACE) 2 in the kidneys of animal models and patients with diabetes suggests ACE2 involvement in diabetic nephrology.
300	20844835	To explore the renoprotective effects of ACE2 overexpression, ACE inhibition (ACEI) or both on diabetic nephropathy and the potential mechanisms involved, 50 Wistar rats were randomly divided into a normal group that received an injection of sodium citrate buffer and a diabetic model group that received an injection of 60 mg/kg streptozotocin.
301	20844835	An experiment in cultured glomerular mesangial cells was performed to examine the effects of ACE2 on cellular proliferation, oxidative stress and collagen IV synthesis.
302	20844835	In comparison with the Ad-GFP group, the Ad-ACE2 group exhibited reduced systolic blood pressure, urinary albumin excretion, creatinine clearance, glomeruli sclerosis index and renal malondialdehyde level; downregulated transforming growth factor (TGF)-β1, vascular endothelial growth factor (VEGF) and collagen IV protein expression; and increased renal superoxide dismutase activity.
303	20844835	ACE2 transfection attenuated angiotensin (Ang) II-induced glomerular mesangial cell proliferation, oxidative stress and collagen IV protein synthesis.
304	20844835	The reduced expression of angiotensin-converting enzyme (ACE) 2 in the kidneys of animal models and patients with diabetes suggests ACE2 involvement in diabetic nephrology.
305	20844835	To explore the renoprotective effects of ACE2 overexpression, ACE inhibition (ACEI) or both on diabetic nephropathy and the potential mechanisms involved, 50 Wistar rats were randomly divided into a normal group that received an injection of sodium citrate buffer and a diabetic model group that received an injection of 60 mg/kg streptozotocin.
306	20844835	An experiment in cultured glomerular mesangial cells was performed to examine the effects of ACE2 on cellular proliferation, oxidative stress and collagen IV synthesis.
307	20844835	In comparison with the Ad-GFP group, the Ad-ACE2 group exhibited reduced systolic blood pressure, urinary albumin excretion, creatinine clearance, glomeruli sclerosis index and renal malondialdehyde level; downregulated transforming growth factor (TGF)-β1, vascular endothelial growth factor (VEGF) and collagen IV protein expression; and increased renal superoxide dismutase activity.
308	20844835	ACE2 transfection attenuated angiotensin (Ang) II-induced glomerular mesangial cell proliferation, oxidative stress and collagen IV protein synthesis.
309	20844835	The reduced expression of angiotensin-converting enzyme (ACE) 2 in the kidneys of animal models and patients with diabetes suggests ACE2 involvement in diabetic nephrology.
310	20844835	To explore the renoprotective effects of ACE2 overexpression, ACE inhibition (ACEI) or both on diabetic nephropathy and the potential mechanisms involved, 50 Wistar rats were randomly divided into a normal group that received an injection of sodium citrate buffer and a diabetic model group that received an injection of 60 mg/kg streptozotocin.
311	20844835	An experiment in cultured glomerular mesangial cells was performed to examine the effects of ACE2 on cellular proliferation, oxidative stress and collagen IV synthesis.
312	20844835	In comparison with the Ad-GFP group, the Ad-ACE2 group exhibited reduced systolic blood pressure, urinary albumin excretion, creatinine clearance, glomeruli sclerosis index and renal malondialdehyde level; downregulated transforming growth factor (TGF)-β1, vascular endothelial growth factor (VEGF) and collagen IV protein expression; and increased renal superoxide dismutase activity.
313	20844835	ACE2 transfection attenuated angiotensin (Ang) II-induced glomerular mesangial cell proliferation, oxidative stress and collagen IV protein synthesis.
314	20844835	The reduced expression of angiotensin-converting enzyme (ACE) 2 in the kidneys of animal models and patients with diabetes suggests ACE2 involvement in diabetic nephrology.
315	20844835	To explore the renoprotective effects of ACE2 overexpression, ACE inhibition (ACEI) or both on diabetic nephropathy and the potential mechanisms involved, 50 Wistar rats were randomly divided into a normal group that received an injection of sodium citrate buffer and a diabetic model group that received an injection of 60 mg/kg streptozotocin.
316	20844835	An experiment in cultured glomerular mesangial cells was performed to examine the effects of ACE2 on cellular proliferation, oxidative stress and collagen IV synthesis.
317	20844835	In comparison with the Ad-GFP group, the Ad-ACE2 group exhibited reduced systolic blood pressure, urinary albumin excretion, creatinine clearance, glomeruli sclerosis index and renal malondialdehyde level; downregulated transforming growth factor (TGF)-β1, vascular endothelial growth factor (VEGF) and collagen IV protein expression; and increased renal superoxide dismutase activity.
318	20844835	ACE2 transfection attenuated angiotensin (Ang) II-induced glomerular mesangial cell proliferation, oxidative stress and collagen IV protein synthesis.
319	20854388	Investigation of ACE, ACE2 and AGTR1 genes for association with nephropathy in Type 1 diabetes mellitus.
320	21115782	ACE2 and diabetes: ACE of ACEs?
321	21381899	The beneficial effects of telmisartan on Angiotensin (Ang)-II mediated oxidative stress and renal fibrosis in streptozotocin (STZ)-induced diabetic nephropathy (DN) were studied.
322	21381899	Compared with NG mice, DG mice showed significant up-regulations of AT-1R, TGF-β1, p-p38MAPK, p-MAPKAPK-2, p-Akt, p47phox, p67phox, gp91phox protein and collagen-III and all of these were significantly reversed in TG mice.
323	21381899	The down-regulated protein expression of Ang-(1-7) mas receptor, ACE-2, PPAR-γ and PGC-1α were observed in DG mice and a significant up-regulation effect of telmisartan has been seen in the TG mice.
324	21670585	Association of angiotensin I converting enzyme, angiotensin II type 1 receptor and angiotensin I converting enzyme 2 gene polymorphisms with the dyslipidemia in type 2 diabetic patients of Chinese Han origin.
325	21792177	Despite evidence that hyperactivity of the vasodeleterious axis (ACE/angiotensin II (Ang II)/AT1 receptor) of the renin-angiotensin system (RAS) is associated with the pathogenesis of diabetic retinopathy (DR) use of the inhibitors of this axis has met with limited success in the control of this pathophysiology.
326	21792177	Diabetes was associated with approximately tenfold and greater than threefold increases in the ratios of ACE/ACE2 and AT1R/Mas mRNA levels in the retina respectively.
327	21845306	[Atorvastatin induced increase in homologous angiotensin I converting enzyme (ACE2) mRNA is associated to decreased fibrosis and decreased left ventricular hypertrophy in a rat model of diabetic cardiomyopathy].
328	22110472	Angiotensin II type II receptor deficiency accelerates the development of nephropathy in type I diabetes via oxidative stress and ACE2.
329	22110472	Renal oxidative stress (measured as heme oxygenase 1 (HO-1) gene expression and reactive oxygen species (ROS) generation) and intrarenal renin angiotensin system components, such as angiotensinogen (Agt), AT(1)R, and angiotensin-converting enzyme (ACE) gene expression, were augmented whereas angiotensin-converting enzyme2 (ACE2) gene expression was decreased in renal proximal tubules (RPTs) of AT(2)RKO mice.
330	22110472	In conclusion, AT(2)R deficiency accelerates the development of DN, which appears to be mediated, at least in part, via heightened oxidative stress and ACE/ACE2 ratio in RPTs.
331	22110472	Angiotensin II type II receptor deficiency accelerates the development of nephropathy in type I diabetes via oxidative stress and ACE2.
332	22110472	Renal oxidative stress (measured as heme oxygenase 1 (HO-1) gene expression and reactive oxygen species (ROS) generation) and intrarenal renin angiotensin system components, such as angiotensinogen (Agt), AT(1)R, and angiotensin-converting enzyme (ACE) gene expression, were augmented whereas angiotensin-converting enzyme2 (ACE2) gene expression was decreased in renal proximal tubules (RPTs) of AT(2)RKO mice.
333	22110472	In conclusion, AT(2)R deficiency accelerates the development of DN, which appears to be mediated, at least in part, via heightened oxidative stress and ACE/ACE2 ratio in RPTs.
334	22110472	Angiotensin II type II receptor deficiency accelerates the development of nephropathy in type I diabetes via oxidative stress and ACE2.
335	22110472	Renal oxidative stress (measured as heme oxygenase 1 (HO-1) gene expression and reactive oxygen species (ROS) generation) and intrarenal renin angiotensin system components, such as angiotensinogen (Agt), AT(1)R, and angiotensin-converting enzyme (ACE) gene expression, were augmented whereas angiotensin-converting enzyme2 (ACE2) gene expression was decreased in renal proximal tubules (RPTs) of AT(2)RKO mice.
336	22110472	In conclusion, AT(2)R deficiency accelerates the development of DN, which appears to be mediated, at least in part, via heightened oxidative stress and ACE/ACE2 ratio in RPTs.
337	22378820	Differential regulation of circulating and renal ACE2 and ACE in hypertensive mRen2.Lewis rats with early-onset diabetes.
338	22378820	Circulating angiotensin-converting enzyme 2 (ACE2) increased ninefold (P < 0.05) in DB females and threefold (P < 0.05) in DB males, but circulating ACE and ANG II were higher in the DB groups.
339	22378820	ACE activity was significantly lower in both female (75%, P < 0.05) and male (50%; P < 0.05) DB groups, while cortical ANG II and Ang-(1-7) levels were unchanged.
340	22378820	In conclusion, female mRen2 rats are not protected from vascular damage, renal inflammation, and kidney injury in early STZ-induced diabetes despite a marked increase in circulating ACE2 and significantly reduced ACE within the kidney.
341	22378820	Differential regulation of circulating and renal ACE2 and ACE in hypertensive mRen2.Lewis rats with early-onset diabetes.
342	22378820	Circulating angiotensin-converting enzyme 2 (ACE2) increased ninefold (P < 0.05) in DB females and threefold (P < 0.05) in DB males, but circulating ACE and ANG II were higher in the DB groups.
343	22378820	ACE activity was significantly lower in both female (75%, P < 0.05) and male (50%; P < 0.05) DB groups, while cortical ANG II and Ang-(1-7) levels were unchanged.
344	22378820	In conclusion, female mRen2 rats are not protected from vascular damage, renal inflammation, and kidney injury in early STZ-induced diabetes despite a marked increase in circulating ACE2 and significantly reduced ACE within the kidney.
345	22378820	Differential regulation of circulating and renal ACE2 and ACE in hypertensive mRen2.Lewis rats with early-onset diabetes.
346	22378820	Circulating angiotensin-converting enzyme 2 (ACE2) increased ninefold (P < 0.05) in DB females and threefold (P < 0.05) in DB males, but circulating ACE and ANG II were higher in the DB groups.
347	22378820	ACE activity was significantly lower in both female (75%, P < 0.05) and male (50%; P < 0.05) DB groups, while cortical ANG II and Ang-(1-7) levels were unchanged.
348	22378820	In conclusion, female mRen2 rats are not protected from vascular damage, renal inflammation, and kidney injury in early STZ-induced diabetes despite a marked increase in circulating ACE2 and significantly reduced ACE within the kidney.
349	22492942	Also, renal levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), ED-1, hypoxia-inducible factor-1α (HIF-1α), and neutrophil gelatinase-associated lipocalin (NGAL) were determined by immunohistochemistry and immunoblotting.
350	22492942	Additionally, ANG-(1-7) reduced renal fibrosis, decreased thiobarbituric acid-reactive substances, and restored the activity of both renal superoxide dismutase and catalase in ZDF.
351	22492942	This attenuation of renal oxidative stress proceeded with decreased renal immunostaining of IL-6, TNF-α, ED-1, HIF-1α, and NGAL to values similar to those displayed by LZR.
352	22492942	Angiotensin-converting enzyme type 2 (ACE2) and ANG II levels remained unchanged after treatment with ANG-(1-7).
353	22536270	Angiotensin-Converting Enzyme 2 (ACE2) Is a Key Modulator of the Renin Angiotensin System in Health and Disease.
354	22536270	Angiotensin-converting enzyme 2 (ACE2) shares some homology with angiotensin-converting enzyme (ACE) but is not inhibited by ACE inhibitors.
355	22536270	The main role of ACE2 is the degradation of Ang II resulting in the formation of angiotensin 1-7 (Ang 1-7) which opposes the actions of Ang II.
356	22536270	Increased Ang II levels are thought to upregulate ACE2 activity, and in ACE2 deficient mice Ang II levels are approximately double that of wild-type mice, whilst Ang 1-7 levels are almost undetectable.
357	22536270	Thus, ACE2 plays a crucial role in the RAS because it opposes the actions of Ang II.
358	22536270	Angiotensin-Converting Enzyme 2 (ACE2) Is a Key Modulator of the Renin Angiotensin System in Health and Disease.
359	22536270	Angiotensin-converting enzyme 2 (ACE2) shares some homology with angiotensin-converting enzyme (ACE) but is not inhibited by ACE inhibitors.
360	22536270	The main role of ACE2 is the degradation of Ang II resulting in the formation of angiotensin 1-7 (Ang 1-7) which opposes the actions of Ang II.
361	22536270	Increased Ang II levels are thought to upregulate ACE2 activity, and in ACE2 deficient mice Ang II levels are approximately double that of wild-type mice, whilst Ang 1-7 levels are almost undetectable.
362	22536270	Thus, ACE2 plays a crucial role in the RAS because it opposes the actions of Ang II.
363	22536270	Angiotensin-Converting Enzyme 2 (ACE2) Is a Key Modulator of the Renin Angiotensin System in Health and Disease.
364	22536270	Angiotensin-converting enzyme 2 (ACE2) shares some homology with angiotensin-converting enzyme (ACE) but is not inhibited by ACE inhibitors.
365	22536270	The main role of ACE2 is the degradation of Ang II resulting in the formation of angiotensin 1-7 (Ang 1-7) which opposes the actions of Ang II.
366	22536270	Increased Ang II levels are thought to upregulate ACE2 activity, and in ACE2 deficient mice Ang II levels are approximately double that of wild-type mice, whilst Ang 1-7 levels are almost undetectable.
367	22536270	Thus, ACE2 plays a crucial role in the RAS because it opposes the actions of Ang II.
368	22536270	Angiotensin-Converting Enzyme 2 (ACE2) Is a Key Modulator of the Renin Angiotensin System in Health and Disease.
369	22536270	Angiotensin-converting enzyme 2 (ACE2) shares some homology with angiotensin-converting enzyme (ACE) but is not inhibited by ACE inhibitors.
370	22536270	The main role of ACE2 is the degradation of Ang II resulting in the formation of angiotensin 1-7 (Ang 1-7) which opposes the actions of Ang II.
371	22536270	Increased Ang II levels are thought to upregulate ACE2 activity, and in ACE2 deficient mice Ang II levels are approximately double that of wild-type mice, whilst Ang 1-7 levels are almost undetectable.
372	22536270	Thus, ACE2 plays a crucial role in the RAS because it opposes the actions of Ang II.
373	22536270	Angiotensin-Converting Enzyme 2 (ACE2) Is a Key Modulator of the Renin Angiotensin System in Health and Disease.
374	22536270	Angiotensin-converting enzyme 2 (ACE2) shares some homology with angiotensin-converting enzyme (ACE) but is not inhibited by ACE inhibitors.
375	22536270	The main role of ACE2 is the degradation of Ang II resulting in the formation of angiotensin 1-7 (Ang 1-7) which opposes the actions of Ang II.
376	22536270	Increased Ang II levels are thought to upregulate ACE2 activity, and in ACE2 deficient mice Ang II levels are approximately double that of wild-type mice, whilst Ang 1-7 levels are almost undetectable.
377	22536270	Thus, ACE2 plays a crucial role in the RAS because it opposes the actions of Ang II.
378	22564510	The role of the renin-angiotensin system in the development of insulin resistance in skeletal muscle.
379	22564510	The canonical renin-angiotensin system (RAS) involves the initial action of renin to cleave angiotensinogen to angiotensin I (ANG I), which is then converted to ANG II by the angiotensin converting enzyme (ACE).
380	22564510	In addition, ANG II, by acting on both endothelial and myocellular AT1 receptors, can induce insulin resistance by increasing cellular oxidative stress, leading to impaired insulin signaling and insulin-stimulated glucose transport activity.
381	22564510	Interventions that target RAS overactivity, including ACE inhibitors, ANG II receptor blockers, and, most recently, renin inhibitors, are effective both in reducing hypertension and in improving whole-body and skeletal muscle insulin action, due at least in part to enhanced Akt-dependent insulin signaling and insulin-dependent glucose transport activity.
382	22564510	ANG-(1-7), which is produced from ANG II by the action of ACE2 and acts via Mas receptors, can counterbalance the deleterious actions of the ACE/ANG II/AT1 receptor axis on the insulin-dependent glucose transport system in skeletal muscle.
383	22564510	This beneficial effect of the ACE2/ANG-(1-7)/Mas receptor axis appears to depend on the activation of Akt.
384	22564510	The role of the renin-angiotensin system in the development of insulin resistance in skeletal muscle.
385	22564510	The canonical renin-angiotensin system (RAS) involves the initial action of renin to cleave angiotensinogen to angiotensin I (ANG I), which is then converted to ANG II by the angiotensin converting enzyme (ACE).
386	22564510	In addition, ANG II, by acting on both endothelial and myocellular AT1 receptors, can induce insulin resistance by increasing cellular oxidative stress, leading to impaired insulin signaling and insulin-stimulated glucose transport activity.
387	22564510	Interventions that target RAS overactivity, including ACE inhibitors, ANG II receptor blockers, and, most recently, renin inhibitors, are effective both in reducing hypertension and in improving whole-body and skeletal muscle insulin action, due at least in part to enhanced Akt-dependent insulin signaling and insulin-dependent glucose transport activity.
388	22564510	ANG-(1-7), which is produced from ANG II by the action of ACE2 and acts via Mas receptors, can counterbalance the deleterious actions of the ACE/ANG II/AT1 receptor axis on the insulin-dependent glucose transport system in skeletal muscle.
389	22564510	This beneficial effect of the ACE2/ANG-(1-7)/Mas receptor axis appears to depend on the activation of Akt.
390	22629438	Angiotensin-converting enzyme 2 (ACE2) is expressed in the kidney and may be a renoprotective enzyme, since it converts angiotensin (Ang) II to Ang-(1-7).
391	22629438	After adjusting for confounding variables, diabetes was significantly associated with urinary ACE2 activity (p = 0.003) and protein levels (p<0.001), while female gender was associated with urinary mRNA levels for both ACE2 and ACE.
392	22629438	Urinary ACE2 could be a marker of renal renin-angiotensin system activation in these patients.
393	22629438	Angiotensin-converting enzyme 2 (ACE2) is expressed in the kidney and may be a renoprotective enzyme, since it converts angiotensin (Ang) II to Ang-(1-7).
394	22629438	After adjusting for confounding variables, diabetes was significantly associated with urinary ACE2 activity (p = 0.003) and protein levels (p<0.001), while female gender was associated with urinary mRNA levels for both ACE2 and ACE.
395	22629438	Urinary ACE2 could be a marker of renal renin-angiotensin system activation in these patients.
396	22629438	Angiotensin-converting enzyme 2 (ACE2) is expressed in the kidney and may be a renoprotective enzyme, since it converts angiotensin (Ang) II to Ang-(1-7).
397	22629438	After adjusting for confounding variables, diabetes was significantly associated with urinary ACE2 activity (p = 0.003) and protein levels (p<0.001), while female gender was associated with urinary mRNA levels for both ACE2 and ACE.
398	22629438	Urinary ACE2 could be a marker of renal renin-angiotensin system activation in these patients.
399	22791320	Podocytes have also been shown to express angiotensin-converting enzyme 2 (ACE2), which can decrease angiotensin II levels by generation of angiotensin-(1-7).
400	23230080	Activation of the ACE2/angiotensin-(1-7)/Mas receptor axis enhances the reparative function of dysfunctional diabetic endothelial progenitors.
401	23230080	We tested the hypothesis that activation of the protective arm of the renin angiotensin system, the angiotensin-converting enzyme 2 (ACE2)/angiotensin-(1-7) [Ang-(1-7)]/Mas receptor axis, corrects the vasoreparative dysfunction typically seen in the CD34(+) cells isolated from diabetic individuals.
402	23230080	The survival and proliferation of CD34(+) cells from diabetic individuals were enhanced by Ang-(1-7) in a Mas/phosphatidylinositol 3-kinase (PI3K)/Akt-dependent manner.
403	23230080	A cohort of patients who remained free of microvascular complications despite having a history of longstanding inadequate glycemic control had higher expression of ACE2/Mas mRNA than patients with diabetes with microvascular complications matched for age, sex, and glycemic control.
404	23230080	Thus, ACE2/Ang-(1-7)Mas pathway activation corrects existing diabetes-induced CD34(+) cell dysfunction and also confers protection from development of this dysfunction.
405	23230080	Activation of the ACE2/angiotensin-(1-7)/Mas receptor axis enhances the reparative function of dysfunctional diabetic endothelial progenitors.
406	23230080	We tested the hypothesis that activation of the protective arm of the renin angiotensin system, the angiotensin-converting enzyme 2 (ACE2)/angiotensin-(1-7) [Ang-(1-7)]/Mas receptor axis, corrects the vasoreparative dysfunction typically seen in the CD34(+) cells isolated from diabetic individuals.
407	23230080	The survival and proliferation of CD34(+) cells from diabetic individuals were enhanced by Ang-(1-7) in a Mas/phosphatidylinositol 3-kinase (PI3K)/Akt-dependent manner.
408	23230080	A cohort of patients who remained free of microvascular complications despite having a history of longstanding inadequate glycemic control had higher expression of ACE2/Mas mRNA than patients with diabetes with microvascular complications matched for age, sex, and glycemic control.
409	23230080	Thus, ACE2/Ang-(1-7)Mas pathway activation corrects existing diabetes-induced CD34(+) cell dysfunction and also confers protection from development of this dysfunction.
410	23230080	Activation of the ACE2/angiotensin-(1-7)/Mas receptor axis enhances the reparative function of dysfunctional diabetic endothelial progenitors.
411	23230080	We tested the hypothesis that activation of the protective arm of the renin angiotensin system, the angiotensin-converting enzyme 2 (ACE2)/angiotensin-(1-7) [Ang-(1-7)]/Mas receptor axis, corrects the vasoreparative dysfunction typically seen in the CD34(+) cells isolated from diabetic individuals.
412	23230080	The survival and proliferation of CD34(+) cells from diabetic individuals were enhanced by Ang-(1-7) in a Mas/phosphatidylinositol 3-kinase (PI3K)/Akt-dependent manner.
413	23230080	A cohort of patients who remained free of microvascular complications despite having a history of longstanding inadequate glycemic control had higher expression of ACE2/Mas mRNA than patients with diabetes with microvascular complications matched for age, sex, and glycemic control.
414	23230080	Thus, ACE2/Ang-(1-7)Mas pathway activation corrects existing diabetes-induced CD34(+) cell dysfunction and also confers protection from development of this dysfunction.
415	23230080	Activation of the ACE2/angiotensin-(1-7)/Mas receptor axis enhances the reparative function of dysfunctional diabetic endothelial progenitors.
416	23230080	We tested the hypothesis that activation of the protective arm of the renin angiotensin system, the angiotensin-converting enzyme 2 (ACE2)/angiotensin-(1-7) [Ang-(1-7)]/Mas receptor axis, corrects the vasoreparative dysfunction typically seen in the CD34(+) cells isolated from diabetic individuals.
417	23230080	The survival and proliferation of CD34(+) cells from diabetic individuals were enhanced by Ang-(1-7) in a Mas/phosphatidylinositol 3-kinase (PI3K)/Akt-dependent manner.
418	23230080	A cohort of patients who remained free of microvascular complications despite having a history of longstanding inadequate glycemic control had higher expression of ACE2/Mas mRNA than patients with diabetes with microvascular complications matched for age, sex, and glycemic control.
419	23230080	Thus, ACE2/Ang-(1-7)Mas pathway activation corrects existing diabetes-induced CD34(+) cell dysfunction and also confers protection from development of this dysfunction.
420	23242734	The renin angiotensin aldosterone system and insulin resistance in humans.
421	23242734	Alterations in the renin angiotensin aldosterone system (RAAS) contribute to the underlying pathophysiology of insulin resistance in humans; however, individual differences in the treatment response of insulin resistance to RAAS blockade persist.
422	23242734	Angiotensin II (ANGII) is the predominant RAAS component contributing to insulin resistance; however, other players such as aldosterone, renin, and ACE2 are also involved.
423	23242734	This review examines the role of local ANGII activity on insulin resistance development in skeletal muscle, adipocytes, and pancreas, followed by a discussion of the other RAAS components implicated in insulin resistance, including ACE2, Ang1-7, renin, and aldosterone.
424	23242734	The renin angiotensin aldosterone system and insulin resistance in humans.
425	23242734	Alterations in the renin angiotensin aldosterone system (RAAS) contribute to the underlying pathophysiology of insulin resistance in humans; however, individual differences in the treatment response of insulin resistance to RAAS blockade persist.
426	23242734	Angiotensin II (ANGII) is the predominant RAAS component contributing to insulin resistance; however, other players such as aldosterone, renin, and ACE2 are also involved.
427	23242734	This review examines the role of local ANGII activity on insulin resistance development in skeletal muscle, adipocytes, and pancreas, followed by a discussion of the other RAAS components implicated in insulin resistance, including ACE2, Ang1-7, renin, and aldosterone.
428	23432153	The enzyme angiotensin-converting enzyme (ACE) converts angiotensin (Ang) I into the vasoconstrictor AngII and was thought, until recently, to be the main effector of the system.
429	23432153	The enzyme ACE2, discovered in 2000, can counterbalance the effects of ACE through degradation of AngII and generation of Ang-(1-7).
430	23432153	Angiotensin-converting enzyme 2 is located on the X-chromosome and circulating ACE2 levels are higher in men than in women.
431	23432153	The enzyme angiotensin-converting enzyme (ACE) converts angiotensin (Ang) I into the vasoconstrictor AngII and was thought, until recently, to be the main effector of the system.
432	23432153	The enzyme ACE2, discovered in 2000, can counterbalance the effects of ACE through degradation of AngII and generation of Ang-(1-7).
433	23432153	Angiotensin-converting enzyme 2 is located on the X-chromosome and circulating ACE2 levels are higher in men than in women.
434	23462816	Pancreatic angiotensin-converting enzyme 2 improves glycemia in angiotensin II-infused mice.
435	23462816	Although ACE2 overexpression has been shown to be protective against the overactive RAS, a role for pancreatic ACE2, particularly in the islets of Langerhans, in regulating glycemia in response to elevated angiotensin II (Ang II) levels remains to be elucidated.
436	23462816	This study examined the role of endogenous pancreatic ACE2 and the impact of elevated Ang II levels on the enzyme's ability to alleviate hyperglycemia in an Ang II infusion mouse model.
437	23462816	Ang II-infused mice exhibited hyperglycemia, hyperinsulinemia, and impaired glucose-stimulated insulin secretion from pancreatic islets compared with control mice.
438	23462816	This phenotype was associated with decreased ACE2 expression and activity, increased Ang II type 1 receptor (AT1R) expression, and increased oxidative stress in the mouse pancreas.
439	23462816	Ad-hACE2 treatment restored pancreatic ACE2 expression and compensatory activity against Ang II-mediated impaired glycemia, thus improving β-cell function.
440	23462816	Pancreatic angiotensin-converting enzyme 2 improves glycemia in angiotensin II-infused mice.
441	23462816	Although ACE2 overexpression has been shown to be protective against the overactive RAS, a role for pancreatic ACE2, particularly in the islets of Langerhans, in regulating glycemia in response to elevated angiotensin II (Ang II) levels remains to be elucidated.
442	23462816	This study examined the role of endogenous pancreatic ACE2 and the impact of elevated Ang II levels on the enzyme's ability to alleviate hyperglycemia in an Ang II infusion mouse model.
443	23462816	Ang II-infused mice exhibited hyperglycemia, hyperinsulinemia, and impaired glucose-stimulated insulin secretion from pancreatic islets compared with control mice.
444	23462816	This phenotype was associated with decreased ACE2 expression and activity, increased Ang II type 1 receptor (AT1R) expression, and increased oxidative stress in the mouse pancreas.
445	23462816	Ad-hACE2 treatment restored pancreatic ACE2 expression and compensatory activity against Ang II-mediated impaired glycemia, thus improving β-cell function.
446	23462816	Pancreatic angiotensin-converting enzyme 2 improves glycemia in angiotensin II-infused mice.
447	23462816	Although ACE2 overexpression has been shown to be protective against the overactive RAS, a role for pancreatic ACE2, particularly in the islets of Langerhans, in regulating glycemia in response to elevated angiotensin II (Ang II) levels remains to be elucidated.
448	23462816	This study examined the role of endogenous pancreatic ACE2 and the impact of elevated Ang II levels on the enzyme's ability to alleviate hyperglycemia in an Ang II infusion mouse model.
449	23462816	Ang II-infused mice exhibited hyperglycemia, hyperinsulinemia, and impaired glucose-stimulated insulin secretion from pancreatic islets compared with control mice.
450	23462816	This phenotype was associated with decreased ACE2 expression and activity, increased Ang II type 1 receptor (AT1R) expression, and increased oxidative stress in the mouse pancreas.
451	23462816	Ad-hACE2 treatment restored pancreatic ACE2 expression and compensatory activity against Ang II-mediated impaired glycemia, thus improving β-cell function.
452	23462816	Pancreatic angiotensin-converting enzyme 2 improves glycemia in angiotensin II-infused mice.
453	23462816	Although ACE2 overexpression has been shown to be protective against the overactive RAS, a role for pancreatic ACE2, particularly in the islets of Langerhans, in regulating glycemia in response to elevated angiotensin II (Ang II) levels remains to be elucidated.
454	23462816	This study examined the role of endogenous pancreatic ACE2 and the impact of elevated Ang II levels on the enzyme's ability to alleviate hyperglycemia in an Ang II infusion mouse model.
455	23462816	Ang II-infused mice exhibited hyperglycemia, hyperinsulinemia, and impaired glucose-stimulated insulin secretion from pancreatic islets compared with control mice.
456	23462816	This phenotype was associated with decreased ACE2 expression and activity, increased Ang II type 1 receptor (AT1R) expression, and increased oxidative stress in the mouse pancreas.
457	23462816	Ad-hACE2 treatment restored pancreatic ACE2 expression and compensatory activity against Ang II-mediated impaired glycemia, thus improving β-cell function.
458	23463883	ACE2, angiotensin-(1–7), and Mas: the other side of the coin.
459	23463883	The renin–angiotensin system (RAS) has recently been extended by the addition of a novel axis consisting of the angiotensin-converting enzyme 2 (ACE2), the heptapeptide angiotensin (1–7) (Ang-(1–7)), and the G protein-coupled receptor Mas.
460	23463883	ACE2 converts the vasoconstrictive and pro-oxidative peptide angiotensin II (Ang II) into Ang-(1–7) which exerts vasodilatory and antioxidative effects via its receptor Mas.
461	23463883	Thereby, ACE2 regulates the local actions of the RAS in cardiovascular tissues and the ACE2/Ang-(1–7)/Mas axis exerts protective actions in hypertension, diabetes, and other cardiovascular disorders.
462	23463883	ACE2, angiotensin-(1–7), and Mas: the other side of the coin.
463	23463883	The renin–angiotensin system (RAS) has recently been extended by the addition of a novel axis consisting of the angiotensin-converting enzyme 2 (ACE2), the heptapeptide angiotensin (1–7) (Ang-(1–7)), and the G protein-coupled receptor Mas.
464	23463883	ACE2 converts the vasoconstrictive and pro-oxidative peptide angiotensin II (Ang II) into Ang-(1–7) which exerts vasodilatory and antioxidative effects via its receptor Mas.
465	23463883	Thereby, ACE2 regulates the local actions of the RAS in cardiovascular tissues and the ACE2/Ang-(1–7)/Mas axis exerts protective actions in hypertension, diabetes, and other cardiovascular disorders.
466	23463883	ACE2, angiotensin-(1–7), and Mas: the other side of the coin.
467	23463883	The renin–angiotensin system (RAS) has recently been extended by the addition of a novel axis consisting of the angiotensin-converting enzyme 2 (ACE2), the heptapeptide angiotensin (1–7) (Ang-(1–7)), and the G protein-coupled receptor Mas.
468	23463883	ACE2 converts the vasoconstrictive and pro-oxidative peptide angiotensin II (Ang II) into Ang-(1–7) which exerts vasodilatory and antioxidative effects via its receptor Mas.
469	23463883	Thereby, ACE2 regulates the local actions of the RAS in cardiovascular tissues and the ACE2/Ang-(1–7)/Mas axis exerts protective actions in hypertension, diabetes, and other cardiovascular disorders.
470	23463883	ACE2, angiotensin-(1–7), and Mas: the other side of the coin.
471	23463883	The renin–angiotensin system (RAS) has recently been extended by the addition of a novel axis consisting of the angiotensin-converting enzyme 2 (ACE2), the heptapeptide angiotensin (1–7) (Ang-(1–7)), and the G protein-coupled receptor Mas.
472	23463883	ACE2 converts the vasoconstrictive and pro-oxidative peptide angiotensin II (Ang II) into Ang-(1–7) which exerts vasodilatory and antioxidative effects via its receptor Mas.
473	23463883	Thereby, ACE2 regulates the local actions of the RAS in cardiovascular tissues and the ACE2/Ang-(1–7)/Mas axis exerts protective actions in hypertension, diabetes, and other cardiovascular disorders.
474	23552863	Overexpression of catalase prevents hypertension and tubulointerstitial fibrosis and normalization of renal angiotensin-converting enzyme-2 expression in Akita mice.
475	23552863	We investigated the relationship among oxidative stress, hypertension, renal injury, and angiotensin-converting enzyme-2 (ACE2) expression in type 1 diabetic Akita mice.
476	23552863	Overexpression of Cat attenuated renal oxidative stress; prevented hypertension; normalized RPTC ACE2 expression and urinary ANG 1-7 levels (both were low in Akita mice); ameliorated glomerular filtration rate, albuminuria, kidney hypertrophy, tubulointerstitial fibrosis, and tubular apoptosis; and suppressed profibrotic and proapoptotic gene expression in RPTCs of Akita Cat-Tg mice compared with Akita mice.
477	23552863	Overexpression of catalase prevents hypertension and tubulointerstitial fibrosis and normalization of renal angiotensin-converting enzyme-2 expression in Akita mice.
478	23552863	We investigated the relationship among oxidative stress, hypertension, renal injury, and angiotensin-converting enzyme-2 (ACE2) expression in type 1 diabetic Akita mice.
479	23552863	Overexpression of Cat attenuated renal oxidative stress; prevented hypertension; normalized RPTC ACE2 expression and urinary ANG 1-7 levels (both were low in Akita mice); ameliorated glomerular filtration rate, albuminuria, kidney hypertrophy, tubulointerstitial fibrosis, and tubular apoptosis; and suppressed profibrotic and proapoptotic gene expression in RPTCs of Akita Cat-Tg mice compared with Akita mice.
480	23646149	Rosiglitazone treatment of type 2 diabetic db/db mice attenuates urinary albumin and angiotensin converting enzyme 2 excretion.
481	23646149	Angiotensin converting enzyme 2 (ACE2) is highly expressed in renal tubules and has been shown to be renoprotective in diabetes.
482	23646149	Renal ACE2 and ADAM17 were significantly increased in db/db mice compared to controls.
483	23646149	We investigated the effect of the insulin sensitizer, rosiglitazone, on albuminuria, renal ADAM17 protein expression and ACE2 shedding in db/db diabetic mice.
484	23646149	Rosiglitazone treatment of db/db mice normalized hyperglycemia, attenuated renal injury and decreased urinary ACE2 and renal ADAM17 protein expression.
485	23646149	Therefore, it is tempting to speculate that renoprotection of rosiglitazone could be partially mediated via downregulation of renal ADAM17 and ACE2 shedding.
486	23646149	In addition, there was a positive correlation between blood glucose, urinary albumin, plasma glucagon, and triglyceride levels with urinary ACE2 excretion.
487	23646149	Rosiglitazone treatment of type 2 diabetic db/db mice attenuates urinary albumin and angiotensin converting enzyme 2 excretion.
488	23646149	Angiotensin converting enzyme 2 (ACE2) is highly expressed in renal tubules and has been shown to be renoprotective in diabetes.
489	23646149	Renal ACE2 and ADAM17 were significantly increased in db/db mice compared to controls.
490	23646149	We investigated the effect of the insulin sensitizer, rosiglitazone, on albuminuria, renal ADAM17 protein expression and ACE2 shedding in db/db diabetic mice.
491	23646149	Rosiglitazone treatment of db/db mice normalized hyperglycemia, attenuated renal injury and decreased urinary ACE2 and renal ADAM17 protein expression.
492	23646149	Therefore, it is tempting to speculate that renoprotection of rosiglitazone could be partially mediated via downregulation of renal ADAM17 and ACE2 shedding.
493	23646149	In addition, there was a positive correlation between blood glucose, urinary albumin, plasma glucagon, and triglyceride levels with urinary ACE2 excretion.
494	23646149	Rosiglitazone treatment of type 2 diabetic db/db mice attenuates urinary albumin and angiotensin converting enzyme 2 excretion.
495	23646149	Angiotensin converting enzyme 2 (ACE2) is highly expressed in renal tubules and has been shown to be renoprotective in diabetes.
496	23646149	Renal ACE2 and ADAM17 were significantly increased in db/db mice compared to controls.
497	23646149	We investigated the effect of the insulin sensitizer, rosiglitazone, on albuminuria, renal ADAM17 protein expression and ACE2 shedding in db/db diabetic mice.
498	23646149	Rosiglitazone treatment of db/db mice normalized hyperglycemia, attenuated renal injury and decreased urinary ACE2 and renal ADAM17 protein expression.
499	23646149	Therefore, it is tempting to speculate that renoprotection of rosiglitazone could be partially mediated via downregulation of renal ADAM17 and ACE2 shedding.
500	23646149	In addition, there was a positive correlation between blood glucose, urinary albumin, plasma glucagon, and triglyceride levels with urinary ACE2 excretion.
501	23646149	Rosiglitazone treatment of type 2 diabetic db/db mice attenuates urinary albumin and angiotensin converting enzyme 2 excretion.
502	23646149	Angiotensin converting enzyme 2 (ACE2) is highly expressed in renal tubules and has been shown to be renoprotective in diabetes.
503	23646149	Renal ACE2 and ADAM17 were significantly increased in db/db mice compared to controls.
504	23646149	We investigated the effect of the insulin sensitizer, rosiglitazone, on albuminuria, renal ADAM17 protein expression and ACE2 shedding in db/db diabetic mice.
505	23646149	Rosiglitazone treatment of db/db mice normalized hyperglycemia, attenuated renal injury and decreased urinary ACE2 and renal ADAM17 protein expression.
506	23646149	Therefore, it is tempting to speculate that renoprotection of rosiglitazone could be partially mediated via downregulation of renal ADAM17 and ACE2 shedding.
507	23646149	In addition, there was a positive correlation between blood glucose, urinary albumin, plasma glucagon, and triglyceride levels with urinary ACE2 excretion.
508	23646149	Rosiglitazone treatment of type 2 diabetic db/db mice attenuates urinary albumin and angiotensin converting enzyme 2 excretion.
509	23646149	Angiotensin converting enzyme 2 (ACE2) is highly expressed in renal tubules and has been shown to be renoprotective in diabetes.
510	23646149	Renal ACE2 and ADAM17 were significantly increased in db/db mice compared to controls.
511	23646149	We investigated the effect of the insulin sensitizer, rosiglitazone, on albuminuria, renal ADAM17 protein expression and ACE2 shedding in db/db diabetic mice.
512	23646149	Rosiglitazone treatment of db/db mice normalized hyperglycemia, attenuated renal injury and decreased urinary ACE2 and renal ADAM17 protein expression.
513	23646149	Therefore, it is tempting to speculate that renoprotection of rosiglitazone could be partially mediated via downregulation of renal ADAM17 and ACE2 shedding.
514	23646149	In addition, there was a positive correlation between blood glucose, urinary albumin, plasma glucagon, and triglyceride levels with urinary ACE2 excretion.
515	23646149	Rosiglitazone treatment of type 2 diabetic db/db mice attenuates urinary albumin and angiotensin converting enzyme 2 excretion.
516	23646149	Angiotensin converting enzyme 2 (ACE2) is highly expressed in renal tubules and has been shown to be renoprotective in diabetes.
517	23646149	Renal ACE2 and ADAM17 were significantly increased in db/db mice compared to controls.
518	23646149	We investigated the effect of the insulin sensitizer, rosiglitazone, on albuminuria, renal ADAM17 protein expression and ACE2 shedding in db/db diabetic mice.
519	23646149	Rosiglitazone treatment of db/db mice normalized hyperglycemia, attenuated renal injury and decreased urinary ACE2 and renal ADAM17 protein expression.
520	23646149	Therefore, it is tempting to speculate that renoprotection of rosiglitazone could be partially mediated via downregulation of renal ADAM17 and ACE2 shedding.
521	23646149	In addition, there was a positive correlation between blood glucose, urinary albumin, plasma glucagon, and triglyceride levels with urinary ACE2 excretion.
522	23658831	BCM7 ameliorated the changes of angiotensin converting enzyme (ACE) and ACE2 levels in the kidney of diabetic rats and BCM7 lowered the levels of angiotensin (Ang)II in the kidney of diabetic rats and culture medium for cells.
523	23671869	The aim of this study was to evaluate the effects of angiotensin-converting enzyme 2 (ACE2) on glucose homeostasis and islet function in mice.
524	23671869	The pancreas was immunohistochemically stained to analyze the relative content of insulin (IRC), vascular endothelial growth factor (VEGF), and microvessel density (MVD) in islets.
525	23671869	There was no difference of body weight, area under curve of glucose (AUCG), area under curve of insulin from 0 to 5 min (AUGI0-5), MVD, and RVC (relative content of VEGF) between WT and ACE2 KO mice with regular chow diet.
526	23671869	The aim of this study was to evaluate the effects of angiotensin-converting enzyme 2 (ACE2) on glucose homeostasis and islet function in mice.
527	23671869	The pancreas was immunohistochemically stained to analyze the relative content of insulin (IRC), vascular endothelial growth factor (VEGF), and microvessel density (MVD) in islets.
528	23671869	There was no difference of body weight, area under curve of glucose (AUCG), area under curve of insulin from 0 to 5 min (AUGI0-5), MVD, and RVC (relative content of VEGF) between WT and ACE2 KO mice with regular chow diet.
529	23714175	Oral Angiotensin-(1-7) prevented obesity and hepatic inflammation by inhibition of resistin/TLR4/MAPK/NF-κB in rats fed with high-fat diet.
530	23714175	RT-PCR evaluated mRNA expression to ACE, ACE2, resistin, TLR4, IL-6, TNF-α and NF-κB genes.
531	23714175	These alterations were accompanied by a marked decreased expression of resistin, TLR4, ACE and increased ACE2 expression in liver.
532	23714175	Oral Angiotensin-(1-7) prevented obesity and hepatic inflammation by inhibition of resistin/TLR4/MAPK/NF-κB in rats fed with high-fat diet.
533	23714175	RT-PCR evaluated mRNA expression to ACE, ACE2, resistin, TLR4, IL-6, TNF-α and NF-κB genes.
534	23714175	These alterations were accompanied by a marked decreased expression of resistin, TLR4, ACE and increased ACE2 expression in liver.
535	23761674	Angiotensin-converting enzyme-2 (ACE2) enhances the degradation of ANG II and its expression is altered in diabetic kidneys, but the regulation of this enzyme in the urine is unknown.
536	23761674	Neither a specific ANG II blocker, telmisartan, nor an ACE inhibitor, captopril, altered the levels of urinary ACE2 in db/db or db/m control mice.
537	23761674	In STZ mice, urinary ACE2 was also increased, and insulin decreased it partly but significantly after several weeks of administration.
538	23761674	Increased urinary ACE2 was associated with more efficient degradation of exogenous ANG II (10(-9) M) in urine from db/db compared with that from db/m mice.
539	23761674	Urinary ACE2 could be a potential biomarker of increased metabolism of ANG II in diabetic kidney disease.
540	23761674	Angiotensin-converting enzyme-2 (ACE2) enhances the degradation of ANG II and its expression is altered in diabetic kidneys, but the regulation of this enzyme in the urine is unknown.
541	23761674	Neither a specific ANG II blocker, telmisartan, nor an ACE inhibitor, captopril, altered the levels of urinary ACE2 in db/db or db/m control mice.
542	23761674	In STZ mice, urinary ACE2 was also increased, and insulin decreased it partly but significantly after several weeks of administration.
543	23761674	Increased urinary ACE2 was associated with more efficient degradation of exogenous ANG II (10(-9) M) in urine from db/db compared with that from db/m mice.
544	23761674	Urinary ACE2 could be a potential biomarker of increased metabolism of ANG II in diabetic kidney disease.
545	23761674	Angiotensin-converting enzyme-2 (ACE2) enhances the degradation of ANG II and its expression is altered in diabetic kidneys, but the regulation of this enzyme in the urine is unknown.
546	23761674	Neither a specific ANG II blocker, telmisartan, nor an ACE inhibitor, captopril, altered the levels of urinary ACE2 in db/db or db/m control mice.
547	23761674	In STZ mice, urinary ACE2 was also increased, and insulin decreased it partly but significantly after several weeks of administration.
548	23761674	Increased urinary ACE2 was associated with more efficient degradation of exogenous ANG II (10(-9) M) in urine from db/db compared with that from db/m mice.
549	23761674	Urinary ACE2 could be a potential biomarker of increased metabolism of ANG II in diabetic kidney disease.
550	23761674	Angiotensin-converting enzyme-2 (ACE2) enhances the degradation of ANG II and its expression is altered in diabetic kidneys, but the regulation of this enzyme in the urine is unknown.
551	23761674	Neither a specific ANG II blocker, telmisartan, nor an ACE inhibitor, captopril, altered the levels of urinary ACE2 in db/db or db/m control mice.
552	23761674	In STZ mice, urinary ACE2 was also increased, and insulin decreased it partly but significantly after several weeks of administration.
553	23761674	Increased urinary ACE2 was associated with more efficient degradation of exogenous ANG II (10(-9) M) in urine from db/db compared with that from db/m mice.
554	23761674	Urinary ACE2 could be a potential biomarker of increased metabolism of ANG II in diabetic kidney disease.
555	23761674	Angiotensin-converting enzyme-2 (ACE2) enhances the degradation of ANG II and its expression is altered in diabetic kidneys, but the regulation of this enzyme in the urine is unknown.
556	23761674	Neither a specific ANG II blocker, telmisartan, nor an ACE inhibitor, captopril, altered the levels of urinary ACE2 in db/db or db/m control mice.
557	23761674	In STZ mice, urinary ACE2 was also increased, and insulin decreased it partly but significantly after several weeks of administration.
558	23761674	Increased urinary ACE2 was associated with more efficient degradation of exogenous ANG II (10(-9) M) in urine from db/db compared with that from db/m mice.
559	23761674	Urinary ACE2 could be a potential biomarker of increased metabolism of ANG II in diabetic kidney disease.
560	23963072	This project was designed to investigate the role of angiotensin converting enzyme 2 (ACE2) in the diabetic renal injury by observing the expression of ACE2 in the kidney and the level of angiotensin II (AngII) in the circulatory system and kidney tissue of rats with diabetes.
561	23963072	The results are as follows: (1) 48-72 h after STZ injection, the rats showed polyuria, polydipsia and their activity reduced. (2) Blood glucose levels were 4.9-6.5 mmol/L in the control rats, 14.0-17.5 mmol/L in the diabetes group rats on the 15th day, and higher than 24 mmol/L in the diabetes group rats on the 30th day; (3) There was a significant increase of urine glucose level (P < 0.05), and a slight but not significant increase of urine protein level (P > 0.05) in the diabetes group on the 15th day; On the 30th day, the levels of urine glucose and urine protein were significantly higher than those in the control group (P < 0.01); (4) Compared with the control group, the expression of ACE2 mRNA was slightly increased (P > 0.05), and the expression of ACE2 protein was significantly increased (P < 0.05) in the rats of diabetic model group on the 15th day; however, on the 30th day, ACE2 mRNA expression in the rats of diabetic model group was significantly lower than the control group (P < 0.05), and the expression of ACE2 protein was slightly lower than the control group (P = 0.0718). (5) Compared with the control group, the levels of AngII in plasma and kidney of the diabetic rats increased slightly on the 15th day (P > 0.05); while the AngII levels in diabetic model group rats were significantly higher (P < 0.05) than that in control rats on the 30th day.
562	23963072	ACE2 expression is reduced gradually with the deepened degree of diabetic kidney damage, leading to the accumulation of AngII in the kidney, thereby increasing the renal injury.
563	23963072	This project was designed to investigate the role of angiotensin converting enzyme 2 (ACE2) in the diabetic renal injury by observing the expression of ACE2 in the kidney and the level of angiotensin II (AngII) in the circulatory system and kidney tissue of rats with diabetes.
564	23963072	The results are as follows: (1) 48-72 h after STZ injection, the rats showed polyuria, polydipsia and their activity reduced. (2) Blood glucose levels were 4.9-6.5 mmol/L in the control rats, 14.0-17.5 mmol/L in the diabetes group rats on the 15th day, and higher than 24 mmol/L in the diabetes group rats on the 30th day; (3) There was a significant increase of urine glucose level (P < 0.05), and a slight but not significant increase of urine protein level (P > 0.05) in the diabetes group on the 15th day; On the 30th day, the levels of urine glucose and urine protein were significantly higher than those in the control group (P < 0.01); (4) Compared with the control group, the expression of ACE2 mRNA was slightly increased (P > 0.05), and the expression of ACE2 protein was significantly increased (P < 0.05) in the rats of diabetic model group on the 15th day; however, on the 30th day, ACE2 mRNA expression in the rats of diabetic model group was significantly lower than the control group (P < 0.05), and the expression of ACE2 protein was slightly lower than the control group (P = 0.0718). (5) Compared with the control group, the levels of AngII in plasma and kidney of the diabetic rats increased slightly on the 15th day (P > 0.05); while the AngII levels in diabetic model group rats were significantly higher (P < 0.05) than that in control rats on the 30th day.
565	23963072	ACE2 expression is reduced gradually with the deepened degree of diabetic kidney damage, leading to the accumulation of AngII in the kidney, thereby increasing the renal injury.
566	23963072	This project was designed to investigate the role of angiotensin converting enzyme 2 (ACE2) in the diabetic renal injury by observing the expression of ACE2 in the kidney and the level of angiotensin II (AngII) in the circulatory system and kidney tissue of rats with diabetes.
567	23963072	The results are as follows: (1) 48-72 h after STZ injection, the rats showed polyuria, polydipsia and their activity reduced. (2) Blood glucose levels were 4.9-6.5 mmol/L in the control rats, 14.0-17.5 mmol/L in the diabetes group rats on the 15th day, and higher than 24 mmol/L in the diabetes group rats on the 30th day; (3) There was a significant increase of urine glucose level (P < 0.05), and a slight but not significant increase of urine protein level (P > 0.05) in the diabetes group on the 15th day; On the 30th day, the levels of urine glucose and urine protein were significantly higher than those in the control group (P < 0.01); (4) Compared with the control group, the expression of ACE2 mRNA was slightly increased (P > 0.05), and the expression of ACE2 protein was significantly increased (P < 0.05) in the rats of diabetic model group on the 15th day; however, on the 30th day, ACE2 mRNA expression in the rats of diabetic model group was significantly lower than the control group (P < 0.05), and the expression of ACE2 protein was slightly lower than the control group (P = 0.0718). (5) Compared with the control group, the levels of AngII in plasma and kidney of the diabetic rats increased slightly on the 15th day (P > 0.05); while the AngII levels in diabetic model group rats were significantly higher (P < 0.05) than that in control rats on the 30th day.
568	23963072	ACE2 expression is reduced gradually with the deepened degree of diabetic kidney damage, leading to the accumulation of AngII in the kidney, thereby increasing the renal injury.