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- W2088516733 abstract "Diabetic nephropathy (DN) is one of the major causes of end-stage renal disease, and previously we demonstrated that NALP3 inflammasome was involved in the pathogenesis of DN. Here we investigated the mechanisms of NALP3 inflammasome activation in podocyte injury during DN. We found that, besides the activation of NALP3 inflammasome and upregulated thioredoxin-interacting protein (TXNIP), the glomerular expression of<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M1><mml:mtext>gp</mml:mtext><mml:msup><mml:mrow><mml:mn>91</mml:mn></mml:mrow><mml:mrow><mml:mi>phox</mml:mi></mml:mrow></mml:msup></mml:math>, a subunit of NADPH oxidase, was enhanced in DN mice simultaneously. Inhibiting NADPH oxidase abrogated NALP3 inflammasome activation, and IL-1 β production and eventually protected podocytes from high glucose- (HG-) induced injury. TXNIP, an inhibitor of thioredoxin, acts as a suppressor for antioxidant defense system. Our observation indicated that in HG-exposed podocytes genetic deletion of TXNIP by shRNA reversed<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M2><mml:mtext>gp</mml:mtext><mml:msup><mml:mrow><mml:mn>91</mml:mn></mml:mrow><mml:mrow><mml:mi>phox</mml:mi></mml:mrow></mml:msup></mml:math>overexpression and alleviated the injury of podocyte. Collectively, our findings proposed that HG-induced NADPH oxidase activation was driven by TXNIP which subsequently triggered NALP3 inflammasome activation in podocytes and ultimately led to podocyte injury, and blocking TXNIP/NADPH oxidase signaling may be a promising treatment for DN. Erratum to “NADPH Oxidase-Induced NALP3 Inflammasome Activation Is Driven by Thioredoxin-Interacting Protein Which Contributes to Podocyte Injury in Hyperglycemia”" @default.
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- W2088516733 date "2015-01-01" @default.
- W2088516733 modified "2023-10-17" @default.
- W2088516733 title "NADPH Oxidase-Induced NALP3 Inflammasome Activation Is Driven by Thioredoxin-Interacting Protein Which Contributes to Podocyte Injury in Hyperglycemia" @default.
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- W2088516733 doi "https://doi.org/10.1155/2015/504761" @default.
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