Ignet

Gene Information

Gene symbol: EZH2

Gene name: enhancer of zeste homolog 2 (Drosophila)

HGNC ID: 3527

Synonyms: EZH1, ENX-1, KMT6, KMT6A

Related Genes

#	Gene Symbol	Number of hits
1	AHCY	1 hits
2	DNMT1	1 hits
3	EGR1	1 hits
4	FOXA1	1 hits
5	FRZB	1 hits
6	HIST3H2A	1 hits
7	JUP	1 hits
8	MARCH8	1 hits
9	MLL3	1 hits
10	MYC	1 hits
11	NLRP3	1 hits
12	PAX2	1 hits
13	PAX6	1 hits
14	PVT1	1 hits
15	RCA1	1 hits
16	SFRP1	1 hits
17	TXNIP	1 hits
18	WT1	1 hits

Related Sentences

#	PMID	Sentence
1	26534922	Here, we investigated the function of the histone methyltransferase enzyme enhancer of zeste homolog 2 (EZH2) in attenuating oxidative injury in podocytes, focusing on its regulation of the endogenous antioxidant inhibitor thioredoxin interacting protein (TxnIP).
2	26534922	Pharmacologic or genetic depletion of EZH2 augmented TxnIP expression and oxidative stress in podocytes cultured under high-glucose conditions.
3	26534922	Conversely, EZH2 upregulation through inhibition of its regulatory microRNA, microRNA-101, downregulated TxnIP and attenuated oxidative stress.
4	26534922	In diabetic rats, depletion of EZH2 decreased histone 3 lysine 27 trimethylation (H3K27me3), increased glomerular TxnIP expression, induced podocyte injury, and augmented oxidative stress and proteinuria.
5	26534922	Chromatin immunoprecipitation sequencing revealed H3K27me3 enrichment at the promoter of the transcription factor Pax6, which was upregulated on EZH2 depletion and bound to the TxnIP promoter, controlling expression of its gene product.
6	26534922	In high glucose-exposed podocytes and the kidneys of diabetic rats, the lower EZH2 expression detected coincided with upregulation of Pax6 and TxnIP.
7	26534922	Finally, in a gene expression array, TxnIP was among seven of 30,854 genes upregulated by high glucose, EZH2 depletion, and the combination thereof.
8	26534922	Thus, EZH2 represses the transcription factor Pax6, which controls expression of the antioxidant inhibitor TxnIP, and in diabetes, downregulation of EZH2 promotes oxidative stress.
9	26534922	Here, we investigated the function of the histone methyltransferase enzyme enhancer of zeste homolog 2 (EZH2) in attenuating oxidative injury in podocytes, focusing on its regulation of the endogenous antioxidant inhibitor thioredoxin interacting protein (TxnIP).
10	26534922	Pharmacologic or genetic depletion of EZH2 augmented TxnIP expression and oxidative stress in podocytes cultured under high-glucose conditions.
11	26534922	Conversely, EZH2 upregulation through inhibition of its regulatory microRNA, microRNA-101, downregulated TxnIP and attenuated oxidative stress.
12	26534922	In diabetic rats, depletion of EZH2 decreased histone 3 lysine 27 trimethylation (H3K27me3), increased glomerular TxnIP expression, induced podocyte injury, and augmented oxidative stress and proteinuria.
13	26534922	Chromatin immunoprecipitation sequencing revealed H3K27me3 enrichment at the promoter of the transcription factor Pax6, which was upregulated on EZH2 depletion and bound to the TxnIP promoter, controlling expression of its gene product.
14	26534922	In high glucose-exposed podocytes and the kidneys of diabetic rats, the lower EZH2 expression detected coincided with upregulation of Pax6 and TxnIP.
15	26534922	Finally, in a gene expression array, TxnIP was among seven of 30,854 genes upregulated by high glucose, EZH2 depletion, and the combination thereof.
16	26534922	Thus, EZH2 represses the transcription factor Pax6, which controls expression of the antioxidant inhibitor TxnIP, and in diabetes, downregulation of EZH2 promotes oxidative stress.
17	26534922	Here, we investigated the function of the histone methyltransferase enzyme enhancer of zeste homolog 2 (EZH2) in attenuating oxidative injury in podocytes, focusing on its regulation of the endogenous antioxidant inhibitor thioredoxin interacting protein (TxnIP).
18	26534922	Pharmacologic or genetic depletion of EZH2 augmented TxnIP expression and oxidative stress in podocytes cultured under high-glucose conditions.
19	26534922	Conversely, EZH2 upregulation through inhibition of its regulatory microRNA, microRNA-101, downregulated TxnIP and attenuated oxidative stress.
20	26534922	In diabetic rats, depletion of EZH2 decreased histone 3 lysine 27 trimethylation (H3K27me3), increased glomerular TxnIP expression, induced podocyte injury, and augmented oxidative stress and proteinuria.
21	26534922	Chromatin immunoprecipitation sequencing revealed H3K27me3 enrichment at the promoter of the transcription factor Pax6, which was upregulated on EZH2 depletion and bound to the TxnIP promoter, controlling expression of its gene product.
22	26534922	In high glucose-exposed podocytes and the kidneys of diabetic rats, the lower EZH2 expression detected coincided with upregulation of Pax6 and TxnIP.
23	26534922	Finally, in a gene expression array, TxnIP was among seven of 30,854 genes upregulated by high glucose, EZH2 depletion, and the combination thereof.
24	26534922	Thus, EZH2 represses the transcription factor Pax6, which controls expression of the antioxidant inhibitor TxnIP, and in diabetes, downregulation of EZH2 promotes oxidative stress.
25	26534922	Here, we investigated the function of the histone methyltransferase enzyme enhancer of zeste homolog 2 (EZH2) in attenuating oxidative injury in podocytes, focusing on its regulation of the endogenous antioxidant inhibitor thioredoxin interacting protein (TxnIP).
26	26534922	Pharmacologic or genetic depletion of EZH2 augmented TxnIP expression and oxidative stress in podocytes cultured under high-glucose conditions.
27	26534922	Conversely, EZH2 upregulation through inhibition of its regulatory microRNA, microRNA-101, downregulated TxnIP and attenuated oxidative stress.
28	26534922	In diabetic rats, depletion of EZH2 decreased histone 3 lysine 27 trimethylation (H3K27me3), increased glomerular TxnIP expression, induced podocyte injury, and augmented oxidative stress and proteinuria.
29	26534922	Chromatin immunoprecipitation sequencing revealed H3K27me3 enrichment at the promoter of the transcription factor Pax6, which was upregulated on EZH2 depletion and bound to the TxnIP promoter, controlling expression of its gene product.
30	26534922	In high glucose-exposed podocytes and the kidneys of diabetic rats, the lower EZH2 expression detected coincided with upregulation of Pax6 and TxnIP.
31	26534922	Finally, in a gene expression array, TxnIP was among seven of 30,854 genes upregulated by high glucose, EZH2 depletion, and the combination thereof.
32	26534922	Thus, EZH2 represses the transcription factor Pax6, which controls expression of the antioxidant inhibitor TxnIP, and in diabetes, downregulation of EZH2 promotes oxidative stress.
33	26534922	Here, we investigated the function of the histone methyltransferase enzyme enhancer of zeste homolog 2 (EZH2) in attenuating oxidative injury in podocytes, focusing on its regulation of the endogenous antioxidant inhibitor thioredoxin interacting protein (TxnIP).
34	26534922	Pharmacologic or genetic depletion of EZH2 augmented TxnIP expression and oxidative stress in podocytes cultured under high-glucose conditions.
35	26534922	Conversely, EZH2 upregulation through inhibition of its regulatory microRNA, microRNA-101, downregulated TxnIP and attenuated oxidative stress.
36	26534922	In diabetic rats, depletion of EZH2 decreased histone 3 lysine 27 trimethylation (H3K27me3), increased glomerular TxnIP expression, induced podocyte injury, and augmented oxidative stress and proteinuria.
37	26534922	Chromatin immunoprecipitation sequencing revealed H3K27me3 enrichment at the promoter of the transcription factor Pax6, which was upregulated on EZH2 depletion and bound to the TxnIP promoter, controlling expression of its gene product.
38	26534922	In high glucose-exposed podocytes and the kidneys of diabetic rats, the lower EZH2 expression detected coincided with upregulation of Pax6 and TxnIP.
39	26534922	Finally, in a gene expression array, TxnIP was among seven of 30,854 genes upregulated by high glucose, EZH2 depletion, and the combination thereof.
40	26534922	Thus, EZH2 represses the transcription factor Pax6, which controls expression of the antioxidant inhibitor TxnIP, and in diabetes, downregulation of EZH2 promotes oxidative stress.
41	26534922	Here, we investigated the function of the histone methyltransferase enzyme enhancer of zeste homolog 2 (EZH2) in attenuating oxidative injury in podocytes, focusing on its regulation of the endogenous antioxidant inhibitor thioredoxin interacting protein (TxnIP).
42	26534922	Pharmacologic or genetic depletion of EZH2 augmented TxnIP expression and oxidative stress in podocytes cultured under high-glucose conditions.
43	26534922	Conversely, EZH2 upregulation through inhibition of its regulatory microRNA, microRNA-101, downregulated TxnIP and attenuated oxidative stress.
44	26534922	In diabetic rats, depletion of EZH2 decreased histone 3 lysine 27 trimethylation (H3K27me3), increased glomerular TxnIP expression, induced podocyte injury, and augmented oxidative stress and proteinuria.
45	26534922	Chromatin immunoprecipitation sequencing revealed H3K27me3 enrichment at the promoter of the transcription factor Pax6, which was upregulated on EZH2 depletion and bound to the TxnIP promoter, controlling expression of its gene product.
46	26534922	In high glucose-exposed podocytes and the kidneys of diabetic rats, the lower EZH2 expression detected coincided with upregulation of Pax6 and TxnIP.
47	26534922	Finally, in a gene expression array, TxnIP was among seven of 30,854 genes upregulated by high glucose, EZH2 depletion, and the combination thereof.
48	26534922	Thus, EZH2 represses the transcription factor Pax6, which controls expression of the antioxidant inhibitor TxnIP, and in diabetes, downregulation of EZH2 promotes oxidative stress.
49	26534922	Here, we investigated the function of the histone methyltransferase enzyme enhancer of zeste homolog 2 (EZH2) in attenuating oxidative injury in podocytes, focusing on its regulation of the endogenous antioxidant inhibitor thioredoxin interacting protein (TxnIP).
50	26534922	Pharmacologic or genetic depletion of EZH2 augmented TxnIP expression and oxidative stress in podocytes cultured under high-glucose conditions.
51	26534922	Conversely, EZH2 upregulation through inhibition of its regulatory microRNA, microRNA-101, downregulated TxnIP and attenuated oxidative stress.
52	26534922	In diabetic rats, depletion of EZH2 decreased histone 3 lysine 27 trimethylation (H3K27me3), increased glomerular TxnIP expression, induced podocyte injury, and augmented oxidative stress and proteinuria.
53	26534922	Chromatin immunoprecipitation sequencing revealed H3K27me3 enrichment at the promoter of the transcription factor Pax6, which was upregulated on EZH2 depletion and bound to the TxnIP promoter, controlling expression of its gene product.
54	26534922	In high glucose-exposed podocytes and the kidneys of diabetic rats, the lower EZH2 expression detected coincided with upregulation of Pax6 and TxnIP.
55	26534922	Finally, in a gene expression array, TxnIP was among seven of 30,854 genes upregulated by high glucose, EZH2 depletion, and the combination thereof.
56	26534922	Thus, EZH2 represses the transcription factor Pax6, which controls expression of the antioxidant inhibitor TxnIP, and in diabetes, downregulation of EZH2 promotes oxidative stress.
57	26534922	Here, we investigated the function of the histone methyltransferase enzyme enhancer of zeste homolog 2 (EZH2) in attenuating oxidative injury in podocytes, focusing on its regulation of the endogenous antioxidant inhibitor thioredoxin interacting protein (TxnIP).
58	26534922	Pharmacologic or genetic depletion of EZH2 augmented TxnIP expression and oxidative stress in podocytes cultured under high-glucose conditions.
59	26534922	Conversely, EZH2 upregulation through inhibition of its regulatory microRNA, microRNA-101, downregulated TxnIP and attenuated oxidative stress.
60	26534922	In diabetic rats, depletion of EZH2 decreased histone 3 lysine 27 trimethylation (H3K27me3), increased glomerular TxnIP expression, induced podocyte injury, and augmented oxidative stress and proteinuria.
61	26534922	Chromatin immunoprecipitation sequencing revealed H3K27me3 enrichment at the promoter of the transcription factor Pax6, which was upregulated on EZH2 depletion and bound to the TxnIP promoter, controlling expression of its gene product.
62	26534922	In high glucose-exposed podocytes and the kidneys of diabetic rats, the lower EZH2 expression detected coincided with upregulation of Pax6 and TxnIP.
63	26534922	Finally, in a gene expression array, TxnIP was among seven of 30,854 genes upregulated by high glucose, EZH2 depletion, and the combination thereof.
64	26534922	Thus, EZH2 represses the transcription factor Pax6, which controls expression of the antioxidant inhibitor TxnIP, and in diabetes, downregulation of EZH2 promotes oxidative stress.
65	28315733	WT1 ameliorates podocyte injury via repression of EZH2/β-catenin pathway in diabetic nephropathy.
66	28315733	Wilm's tumor 1 (WT1) has been found to have opposing roles with β-catenin in podocyte biology.
67	28315733	Herein, we asked whether the histone methyltransferase enzyme enhancer of zeste homolog 2 (EZH2) promotes WT1-induced podocyte injury via β-catenin activation and the underlying mechanisms.
68	28315733	We found that WT1 antagonized EZH2 and ameliorated β-catenin-mediated podocyte injury as demonstrated by attenuated podocyte mesenchymal transition, maintenance of podocyte architectural integrity, decreased podocyte apoptosis and oxidative stress.
69	28315733	Further, we provided mechanistical evidence that EZH2 was required in WT1-mediated β-catenin inactivation via repression of secreted frizzled-related protein 1 (SFRP-1), a Wnt antagonist.
70	28315733	Moreover, EZH2-mediated silencing of SFRP-1 was due to increased histone 3 lysine 27 trimethylation (H3K27me3) on its promoter region.
71	28315733	We propose an epigenetic process via the WT1/EZH2/β-catenin axis in attenuating podocyte injury in DN.
72	28315733	Targeting WT1 and EZH2 could be potential therapeutic approaches for DN.
73	28315733	WT1 ameliorates podocyte injury via repression of EZH2/β-catenin pathway in diabetic nephropathy.
74	28315733	Wilm's tumor 1 (WT1) has been found to have opposing roles with β-catenin in podocyte biology.
75	28315733	Herein, we asked whether the histone methyltransferase enzyme enhancer of zeste homolog 2 (EZH2) promotes WT1-induced podocyte injury via β-catenin activation and the underlying mechanisms.
76	28315733	We found that WT1 antagonized EZH2 and ameliorated β-catenin-mediated podocyte injury as demonstrated by attenuated podocyte mesenchymal transition, maintenance of podocyte architectural integrity, decreased podocyte apoptosis and oxidative stress.
77	28315733	Further, we provided mechanistical evidence that EZH2 was required in WT1-mediated β-catenin inactivation via repression of secreted frizzled-related protein 1 (SFRP-1), a Wnt antagonist.
78	28315733	Moreover, EZH2-mediated silencing of SFRP-1 was due to increased histone 3 lysine 27 trimethylation (H3K27me3) on its promoter region.
79	28315733	We propose an epigenetic process via the WT1/EZH2/β-catenin axis in attenuating podocyte injury in DN.
80	28315733	Targeting WT1 and EZH2 could be potential therapeutic approaches for DN.
81	28315733	WT1 ameliorates podocyte injury via repression of EZH2/β-catenin pathway in diabetic nephropathy.
82	28315733	Wilm's tumor 1 (WT1) has been found to have opposing roles with β-catenin in podocyte biology.
83	28315733	Herein, we asked whether the histone methyltransferase enzyme enhancer of zeste homolog 2 (EZH2) promotes WT1-induced podocyte injury via β-catenin activation and the underlying mechanisms.
84	28315733	We found that WT1 antagonized EZH2 and ameliorated β-catenin-mediated podocyte injury as demonstrated by attenuated podocyte mesenchymal transition, maintenance of podocyte architectural integrity, decreased podocyte apoptosis and oxidative stress.
85	28315733	Further, we provided mechanistical evidence that EZH2 was required in WT1-mediated β-catenin inactivation via repression of secreted frizzled-related protein 1 (SFRP-1), a Wnt antagonist.
86	28315733	Moreover, EZH2-mediated silencing of SFRP-1 was due to increased histone 3 lysine 27 trimethylation (H3K27me3) on its promoter region.
87	28315733	We propose an epigenetic process via the WT1/EZH2/β-catenin axis in attenuating podocyte injury in DN.
88	28315733	Targeting WT1 and EZH2 could be potential therapeutic approaches for DN.
89	28315733	WT1 ameliorates podocyte injury via repression of EZH2/β-catenin pathway in diabetic nephropathy.
90	28315733	Wilm's tumor 1 (WT1) has been found to have opposing roles with β-catenin in podocyte biology.
91	28315733	Herein, we asked whether the histone methyltransferase enzyme enhancer of zeste homolog 2 (EZH2) promotes WT1-induced podocyte injury via β-catenin activation and the underlying mechanisms.
92	28315733	We found that WT1 antagonized EZH2 and ameliorated β-catenin-mediated podocyte injury as demonstrated by attenuated podocyte mesenchymal transition, maintenance of podocyte architectural integrity, decreased podocyte apoptosis and oxidative stress.
93	28315733	Further, we provided mechanistical evidence that EZH2 was required in WT1-mediated β-catenin inactivation via repression of secreted frizzled-related protein 1 (SFRP-1), a Wnt antagonist.
94	28315733	Moreover, EZH2-mediated silencing of SFRP-1 was due to increased histone 3 lysine 27 trimethylation (H3K27me3) on its promoter region.
95	28315733	We propose an epigenetic process via the WT1/EZH2/β-catenin axis in attenuating podocyte injury in DN.
96	28315733	Targeting WT1 and EZH2 could be potential therapeutic approaches for DN.
97	28315733	WT1 ameliorates podocyte injury via repression of EZH2/β-catenin pathway in diabetic nephropathy.
98	28315733	Wilm's tumor 1 (WT1) has been found to have opposing roles with β-catenin in podocyte biology.
99	28315733	Herein, we asked whether the histone methyltransferase enzyme enhancer of zeste homolog 2 (EZH2) promotes WT1-induced podocyte injury via β-catenin activation and the underlying mechanisms.
100	28315733	We found that WT1 antagonized EZH2 and ameliorated β-catenin-mediated podocyte injury as demonstrated by attenuated podocyte mesenchymal transition, maintenance of podocyte architectural integrity, decreased podocyte apoptosis and oxidative stress.
101	28315733	Further, we provided mechanistical evidence that EZH2 was required in WT1-mediated β-catenin inactivation via repression of secreted frizzled-related protein 1 (SFRP-1), a Wnt antagonist.
102	28315733	Moreover, EZH2-mediated silencing of SFRP-1 was due to increased histone 3 lysine 27 trimethylation (H3K27me3) on its promoter region.
103	28315733	We propose an epigenetic process via the WT1/EZH2/β-catenin axis in attenuating podocyte injury in DN.
104	28315733	Targeting WT1 and EZH2 could be potential therapeutic approaches for DN.
105	28315733	WT1 ameliorates podocyte injury via repression of EZH2/β-catenin pathway in diabetic nephropathy.
106	28315733	Wilm's tumor 1 (WT1) has been found to have opposing roles with β-catenin in podocyte biology.
107	28315733	Herein, we asked whether the histone methyltransferase enzyme enhancer of zeste homolog 2 (EZH2) promotes WT1-induced podocyte injury via β-catenin activation and the underlying mechanisms.
108	28315733	We found that WT1 antagonized EZH2 and ameliorated β-catenin-mediated podocyte injury as demonstrated by attenuated podocyte mesenchymal transition, maintenance of podocyte architectural integrity, decreased podocyte apoptosis and oxidative stress.
109	28315733	Further, we provided mechanistical evidence that EZH2 was required in WT1-mediated β-catenin inactivation via repression of secreted frizzled-related protein 1 (SFRP-1), a Wnt antagonist.
110	28315733	Moreover, EZH2-mediated silencing of SFRP-1 was due to increased histone 3 lysine 27 trimethylation (H3K27me3) on its promoter region.
111	28315733	We propose an epigenetic process via the WT1/EZH2/β-catenin axis in attenuating podocyte injury in DN.
112	28315733	Targeting WT1 and EZH2 could be potential therapeutic approaches for DN.
113	28315733	WT1 ameliorates podocyte injury via repression of EZH2/β-catenin pathway in diabetic nephropathy.
114	28315733	Wilm's tumor 1 (WT1) has been found to have opposing roles with β-catenin in podocyte biology.
115	28315733	Herein, we asked whether the histone methyltransferase enzyme enhancer of zeste homolog 2 (EZH2) promotes WT1-induced podocyte injury via β-catenin activation and the underlying mechanisms.
116	28315733	We found that WT1 antagonized EZH2 and ameliorated β-catenin-mediated podocyte injury as demonstrated by attenuated podocyte mesenchymal transition, maintenance of podocyte architectural integrity, decreased podocyte apoptosis and oxidative stress.
117	28315733	Further, we provided mechanistical evidence that EZH2 was required in WT1-mediated β-catenin inactivation via repression of secreted frizzled-related protein 1 (SFRP-1), a Wnt antagonist.
118	28315733	Moreover, EZH2-mediated silencing of SFRP-1 was due to increased histone 3 lysine 27 trimethylation (H3K27me3) on its promoter region.
119	28315733	We propose an epigenetic process via the WT1/EZH2/β-catenin axis in attenuating podocyte injury in DN.
120	28315733	Targeting WT1 and EZH2 could be potential therapeutic approaches for DN.
121	29357419	Modulation of apolipoprotein L1-microRNA-193a axis prevents podocyte dedifferentiation in high-glucose milieu.
122	29357419	HG-induced DPD dedifferentiation manifested in the form of downregulation of Wilms' tumor 1 (WT1) and upregulation of paired box 2 (PAX2) expression.
123	29357419	WT1-silenced DPDs displayed enhanced expression of PAX2.
124	29357419	Immunoprecipitation of DPD cellular lysates with anti-WT1 antibody revealed formation of WT1 repressor complexes containing Polycomb group proteins, enhancer of zeste homolog 2, menin, and DNA methyltransferase (DNMT1), whereas silencing of either WT1 or DNMT1 disrupted this complex with enhanced expression of PAX2.
125	29357419	HG downregulated DPD expression of APOL1. miR193a-overexpressing DPDs displayed downregulation of APOL1 and enhanced expression of dedifferentiating markers; conversely, silencing of miR193a enhanced the expression of APOL1 and preserved DPD phenotype.
126	29357419	Moreover, stably APOL1G0-overexpressing DPDs displayed the enhanced expression of WT1 but attenuated expression of miR193a; nonetheless, silencing of APOL1 reversed these effects.
127	29357419	Vitamin D receptor agonist downregulated miR193a, upregulated APOL1 expression, and prevented dedifferentiation of DPDs in HG milieu.
128	31371698	Silencing of long noncoding RNA PVT1 inhibits podocyte damage and apoptosis in diabetic nephropathy by upregulating FOXA1.
129	31371698	Herein, we aimed to study the roles of long noncoding RNA (lncRNA) plasmacytoma variant translocation 1 (PVT1) and histone 3 lysine 27 trimethylation (H3K27me3) in DN.
130	31371698	The roles of PVT1 and enhancer of zeste homolog 2 (EZH2) were validated via loss-of-function and gain-of-function in vitro experiments to identify the interactions among PVT1, EZH2, and forkhead box A1 (FOXA1).
131	31371698	The podocyte damage and apoptosis due to PVT1 and FOXA1 were verified with in vivo experiments.
132	31371698	A large number of CpG (C-phosphate-G) island sites were predicted at the FOXA1 promoter region, where PVT1 recruited EZH2 to promote the recruitment of H3K27me3.
133	31371698	The silencing of PVT1 or the overexpression of FOXA1 relieved the damage and inhibited the apoptosis of podocytes in DN, as was evidenced by the upregulated expression of synaptopodin and podocin, higher expression of Bcl-2, and lower expression of Bax and cleaved caspase-3.
134	31371698	The key findings of this study collectively indicate that the suppression of lncRNA PVT1 exerts inhibitory effects on podocyte damage and apoptosis via FOXA1 in DN, which is of clinical significance.
135	31371698	Silencing of long noncoding RNA PVT1 inhibits podocyte damage and apoptosis in diabetic nephropathy by upregulating FOXA1.
136	31371698	Herein, we aimed to study the roles of long noncoding RNA (lncRNA) plasmacytoma variant translocation 1 (PVT1) and histone 3 lysine 27 trimethylation (H3K27me3) in DN.
137	31371698	The roles of PVT1 and enhancer of zeste homolog 2 (EZH2) were validated via loss-of-function and gain-of-function in vitro experiments to identify the interactions among PVT1, EZH2, and forkhead box A1 (FOXA1).
138	31371698	The podocyte damage and apoptosis due to PVT1 and FOXA1 were verified with in vivo experiments.
139	31371698	A large number of CpG (C-phosphate-G) island sites were predicted at the FOXA1 promoter region, where PVT1 recruited EZH2 to promote the recruitment of H3K27me3.
140	31371698	The silencing of PVT1 or the overexpression of FOXA1 relieved the damage and inhibited the apoptosis of podocytes in DN, as was evidenced by the upregulated expression of synaptopodin and podocin, higher expression of Bcl-2, and lower expression of Bax and cleaved caspase-3.
141	31371698	The key findings of this study collectively indicate that the suppression of lncRNA PVT1 exerts inhibitory effects on podocyte damage and apoptosis via FOXA1 in DN, which is of clinical significance.
142	33679454	Enhancer of zeste homolog 2 (EZH2) is a histone-lysine N-methyltransferase enzyme that catalyzes the addition of methyl groups to histone H3 at lysine 27, leading to gene silencing.
143	33679454	Mutation or over-expression of EZH2 has been linked to many cancers including renal carcinoma.
144	33679454	Enhancer of zeste homolog 2 (EZH2) is a histone-lysine N-methyltransferase enzyme that catalyzes the addition of methyl groups to histone H3 at lysine 27, leading to gene silencing.
145	33679454	Mutation or over-expression of EZH2 has been linked to many cancers including renal carcinoma.
146	34057794	Homocysteine induces podocyte apoptosis by regulating miR-1929-5p expression through c-Myc, DNMT1 and EZH2.
147	34057794	Hcy upregulated DNA methyltransferase 1 (DNMT1) and enhancer of zeste homolog 2 (EZH2) levels, resulting in increased DNA methylation and H3K27me3 levels on the miR-1929-5p promoter.
148	34057794	Additionally, we observed that c-Myc recruited DNMT1 and EZH2 to the miR-1929-5p promoter and suppressed the expression of miR-1929-5p.
149	34057794	In summary, we demonstrated that Hcy promotes podocyte apoptosis through the regulation of the epigenetic modifiers DNMT1 and EZH2, which are recruited by c-Myc to the promoter of miR-1929-5p to silence miR-1929-5p expression.
150	34057794	Homocysteine induces podocyte apoptosis by regulating miR-1929-5p expression through c-Myc, DNMT1 and EZH2.
151	34057794	Hcy upregulated DNA methyltransferase 1 (DNMT1) and enhancer of zeste homolog 2 (EZH2) levels, resulting in increased DNA methylation and H3K27me3 levels on the miR-1929-5p promoter.
152	34057794	Additionally, we observed that c-Myc recruited DNMT1 and EZH2 to the miR-1929-5p promoter and suppressed the expression of miR-1929-5p.
153	34057794	In summary, we demonstrated that Hcy promotes podocyte apoptosis through the regulation of the epigenetic modifiers DNMT1 and EZH2, which are recruited by c-Myc to the promoter of miR-1929-5p to silence miR-1929-5p expression.
154	34057794	Homocysteine induces podocyte apoptosis by regulating miR-1929-5p expression through c-Myc, DNMT1 and EZH2.
155	34057794	Hcy upregulated DNA methyltransferase 1 (DNMT1) and enhancer of zeste homolog 2 (EZH2) levels, resulting in increased DNA methylation and H3K27me3 levels on the miR-1929-5p promoter.
156	34057794	Additionally, we observed that c-Myc recruited DNMT1 and EZH2 to the miR-1929-5p promoter and suppressed the expression of miR-1929-5p.
157	34057794	In summary, we demonstrated that Hcy promotes podocyte apoptosis through the regulation of the epigenetic modifiers DNMT1 and EZH2, which are recruited by c-Myc to the promoter of miR-1929-5p to silence miR-1929-5p expression.
158	34057794	Homocysteine induces podocyte apoptosis by regulating miR-1929-5p expression through c-Myc, DNMT1 and EZH2.
159	34057794	Hcy upregulated DNA methyltransferase 1 (DNMT1) and enhancer of zeste homolog 2 (EZH2) levels, resulting in increased DNA methylation and H3K27me3 levels on the miR-1929-5p promoter.
160	34057794	Additionally, we observed that c-Myc recruited DNMT1 and EZH2 to the miR-1929-5p promoter and suppressed the expression of miR-1929-5p.
161	34057794	In summary, we demonstrated that Hcy promotes podocyte apoptosis through the regulation of the epigenetic modifiers DNMT1 and EZH2, which are recruited by c-Myc to the promoter of miR-1929-5p to silence miR-1929-5p expression.
162	34119876	Epigenetic regulation of TXNIP-mediated oxidative stress and NLRP3 inflammasome activation contributes to SAHH inhibition-aggravated diabetic nephropathy.
163	34119876	In the present study, we found that inhibition of SAHH by using its inhibitor adenosine dialdehyde (ADA) accumulates intracellular or plasma SAH levels and increases high glucose-induced podocyte injury and aggravates STZ-induced diabetic nephropathy, which is associated with Nod-like receptor protein 3 (NLRP3) inflammasome activation.
164	34119876	Inhibition or knockout of NLRP3 attenuates SAHH inhibition-aggravated podocyte injury and diabetic nephropathy.
165	34119876	Additionally, SAHH inhibition increases thioredoxin-interacting protein (TXNIP)-mediated oxidative stress and NLRP3 inflammasome activation, but these effects were not observed in TXNIP knockout mice.
166	34119876	Mechanistically, SAHH inhibition increased TXNIP by inhibiting histone methyltransferase enhancer of zeste homolog 2 (EZH2) and reduced trimethylation of histone H3 lysine 27 and its enrichment at promoter of early growth response 1 (EGR1).
167	34119876	Moreover, EGR1 is activated and enriched at promoters of TXNIP by SAHH inhibition and is essential for SAHH inhibition-induced TXNIP expression.
168	34119876	Inhibition of EGR1 protected against SAHH inhibition-induced NLRP3 inflammasome activation and oxidative stress and diabetic nephropathy.
169	34119876	These findings suggest that EZH2/EGR1/TXNIP/NLRP3 signaling cascade contributes to SAHH inhibition-aggravated diabetic nephropathy.
170	34119876	Epigenetic regulation of TXNIP-mediated oxidative stress and NLRP3 inflammasome activation contributes to SAHH inhibition-aggravated diabetic nephropathy.
171	34119876	In the present study, we found that inhibition of SAHH by using its inhibitor adenosine dialdehyde (ADA) accumulates intracellular or plasma SAH levels and increases high glucose-induced podocyte injury and aggravates STZ-induced diabetic nephropathy, which is associated with Nod-like receptor protein 3 (NLRP3) inflammasome activation.
172	34119876	Inhibition or knockout of NLRP3 attenuates SAHH inhibition-aggravated podocyte injury and diabetic nephropathy.
173	34119876	Additionally, SAHH inhibition increases thioredoxin-interacting protein (TXNIP)-mediated oxidative stress and NLRP3 inflammasome activation, but these effects were not observed in TXNIP knockout mice.
174	34119876	Mechanistically, SAHH inhibition increased TXNIP by inhibiting histone methyltransferase enhancer of zeste homolog 2 (EZH2) and reduced trimethylation of histone H3 lysine 27 and its enrichment at promoter of early growth response 1 (EGR1).
175	34119876	Moreover, EGR1 is activated and enriched at promoters of TXNIP by SAHH inhibition and is essential for SAHH inhibition-induced TXNIP expression.
176	34119876	Inhibition of EGR1 protected against SAHH inhibition-induced NLRP3 inflammasome activation and oxidative stress and diabetic nephropathy.
177	34119876	These findings suggest that EZH2/EGR1/TXNIP/NLRP3 signaling cascade contributes to SAHH inhibition-aggravated diabetic nephropathy.