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PMID |
Sentence |
1 |
29064158
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Treatment of mouse mesangial cells with THSG induced nuclear factor erythroid-derived 2-like 2 (Nrf2) nuclear translocation, increased heme oxygenase-1 and NAD(P)H:quinone oxidoreductase (NQO)-1 gene expressions, and reduced cellular thiol oxidation and resistance to AD-induced cytotoxicity.
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2 |
29064158
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Silencing Nrf2 and its repressor protein, Kelch-like ECH-associated protein 1 (Keap1), abolished these protective effects of THSG.
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3 |
31325480
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BRD4 contributes to high-glucose-induced podocyte injury by modulating Keap1/Nrf2/ARE signaling.
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4 |
31325480
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Bromodomain-containing protein 4 (BRD4) has emerged as a critical regulator for cell injury.
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5 |
31325480
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Moreover, BRD4 inhibition potentiated nuclear factor (erythroid-derived 2)-like 2 (Nrf2) signaling associated with suppression of Kelch-like ECH-associated protein (Keap1).
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6 |
31325480
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BRD4 inhibition promoted Nrf2 nuclear translocation and upregulated the transcriptional activity of Nrf2/antioxidant response element (ARE).
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7 |
31325480
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Overall, these results suggest that BRD4 inhibition confers cytoprotection against HG injury in podocytes through potentiation of Nrf2/ARE antioxidant signaling.
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8 |
31325480
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This finding implicates BRD4/Nrf2/ARE signaling in the pathogenesis of diabetic nephropathy.
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9 |
32238837
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Linagliptin affects IRS1/Akt signaling and prevents high glucose-induced apoptosis in podocytes.
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10 |
32238837
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Furthermore, linagliptin improved insulin-induced phosphorylation of insulin receptor substrate 1 (IRS1) and Akt, which was inhibited in high-glucose conditions.
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11 |
32238837
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Because reactive oxygen species inhibit glomerular insulin signalling in diabetes and Kelch-like ECH-associated protein 1 (Keap1)/nuclear factor erythroid 2-related factor 2 (Nrf2) pathway is one of the most important intrinsic antioxidative systems, we evaluated whether linagliptin increased Nrf2 in podocytes.
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12 |
32238837
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In summary, linagliptin offers protection against DKD by enhancing IRS1/Akt insulin signalling in podocytes and partially via the Keap1/Nrf2 pathway.
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13 |
32818518
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The nuclear factor erythroid 2-related factor 2 (Nrf2) pathway upregulates key cellular defenses.
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14 |
32818518
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To understand this effect, we examined genetically engineered mice with elevated Nrf2 signaling due to reduced expression of the Nrf2 inhibitor, Kelch-like ECH-associated protein 1 (Keap1).
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15 |
32818518
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These Keap1FA/FA mice lacked baseline proteinuria but exhibited increased proteinuria in experimental models evoked by adriamycin, angiotensin II, or protein overload.
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16 |
32818518
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After injury, Keap1FA/FA mice had increased glomerulosclerosis, nephrin disruption and shedding, podocyte injury, foot process effacement, and interstitial fibrosis.
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17 |
32818518
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Compared to angiotensin II alone, the combination of angiotensin II and CDDO-Im significantly increased proteinuria, a phenomenon not observed in Nrf2 knockout mice.
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18 |
34426758
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Moreover, MitoQ rescued the expression and translocation of Nrf2 (nuclear factor E2-related factor 2) and decreased the expression of Keap1 (Kelch-like ECH-associated protein 1) in Ang II-stimulated podocytes.
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19 |
34426758
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Nrf2 knockdown partially blocked the protective effects of MitoQ on Ang II-induced mitochondrial fission and oxidative stress in podocytes.
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20 |
34931430
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Inhibition of USP15 ameliorates high-glucose-induced oxidative stress and inflammatory injury in podocytes through regulation of the Keap1/Nrf2 signaling.
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21 |
34931430
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Ubiquitin-specific peptidase 15 (USP15) is implicated in the pathogenesis of numerous diseases.
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22 |
34931430
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Further investigation showed that inhibition of USP15 enhanced the activation of NF-E2-related factor 2 (Nrf2) and expression of Nrf2 target genes in HG-simulated podocytes.
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23 |
34931430
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Moreover, depletion of Kelch-like ECH-associated protein 1 (Keap1) diminished the regulatory effect of USP15 inhibition on Nrf2 activation.
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24 |
34931430
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Taken together, these data indicate that USP15 inhibition protects podocytes from HG-induced injury by enhancing Nrf2 activation via Keap1.
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