Smad4 promotes diabetic nephropathy by modulating glycolysis and OXPHOS.
作者： Jinhua Li , Yu Bo Yang Sun , Weiyi Chen , Jinjin Fan , Songhui Li
关键词:
摘要: Diabetic nephropathy (DN) is the leading cause of end‐stage kidney disease. TGF‐β1/Smad3 signalling plays a major pathological role in DN; however, the contribution of Smad4 has not been examined. Smad4 depletion in the kidney using anti‐Smad4 locked nucleic acid halted progressive podocyte damage and glomerulosclerosis in mouse type 2 DN, suggesting a pathogenic role of Smad4 in podocytes. Smad4 is upregulated in human and mouse podocytes during DN. Conditional Smad4 deletion in podocytes protects mice …
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