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- W2081569453 abstract "Injury to podocytes leads to the onset of chronic renal diseases characterized by proteinuria. Elevated transforming growth factor (TGF)-β in kidney tissue is associated with podocyte damage that ultimately results in apoptosis and detachment. We investigated the proapoptotic mechanism of TGF-β in immortalized mouse podocytes. Exogenous TGF-β 1 -induced podocyte apoptosis through caspase-3 activation, which was related to elevated ROS levels generated by selective upregulation of NADPH oxidase 4 (Nox4). In mouse podocytes, Nox4 was predominantly localized to mitochondria, and Nox4 upregulation by TGF-β 1 markedly depolarized mitochondrial membrane potential. TGF-β 1 -induced ROS production and caspase activation were mitigated by an antioxidant, the Nox inhibitor diphenyleneiodonium, or small interfering RNA for Nox4. A TGF-β receptor I blocker, SB-431542, completely reversed the changes triggered by TGF-β 1 . Knockdown of either Smad2 or Smad3 prevented the increase of Nox4 expression, ROS generation, loss of mitochondrial membrane potential, and caspase-3 activation by TGF-β 1 . These results suggest that TGF-β 1 -induced mitochondrial Nox4 upregulation via the TGF-β receptor-Smad2/3 pathway is responsible for ROS production, mitochondrial dysfunction, and apoptosis, which may at least in part contribute to the development and progression of proteinuric glomerular diseases such as diabetic nephropathy." @default.
- W2081569453 created "2016-06-24" @default.
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- W2081569453 date "2014-01-15" @default.
- W2081569453 modified "2023-09-30" @default.
- W2081569453 title "Upregulation of mitochondrial Nox4 mediates TGF-β-induced apoptosis in cultured mouse podocytes" @default.
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- W2081569453 doi "https://doi.org/10.1152/ajprenal.00438.2013" @default.
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