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• W2015930811 abstract "Proteinuria is an independent risk factor for end-stage renal disease (ESRD) (Shankland, 2006). Recent studies highlighted the mechanisms of podocyte injury and implications for potential treatment strategies in proteinuric kidney diseases (Zhang et al., 2012). Reactive oxygen species (ROS) are cellular signals which are closely associated with the development and progression of glomerular sclerosis. NADPH oxidase is a district enzymatic source of cellular ROS production and prominently expressed in podocytes (Zhang et al., 2010). In the last decade, it has become evident that NADPH oxidase-derived ROS overproduction is a key trigger of podocyte injury, such as renin-angiotensin-aldosterone system activation (Whaley-Connell et al., 2006), epithelial-to-mesenchymal transition (Zhang et al., 2011), and inflammatory priming (Abais et al., 2013). This review focuses on the mechanism of NADPH oxidase-mediated ROS in podocyte injury under different pathophysiological conditions. In addition, we also reviewed the therapeutic perspectives of NADPH oxidase in kidney diseases related to podocyte injury." @default.
• W2015930811 created "2016-06-24" @default.
• W2015930811 creator A5002797149 @default.
• W2015930811 creator A5032437498 @default.
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• W2015930811 date "2013-01-01" @default.
• W2015930811 modified "2023-10-17" @default.
• W2015930811 title "Role of NADPH Oxidase-Mediated Reactive Oxygen Species in Podocyte Injury" @default.
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• W2015930811 doi "https://doi.org/10.1155/2013/839761" @default.
• W2015930811 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3844218" @default.
• W2015930811 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24319690" @default.
• W2015930811 hasPublicationYear "2013" @default.
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