Resveratrol ameliorates podocyte damage in diabetic mice via SIRT1/PGC‐1α mediated attenuation of mitochondrial oxidative stress

• Published in: Journal of cellular physiology Vol. 234; no. 4; pp. 5033 - 5043
• Main Authors: Zhang, Tao, Chi, Yanqing, Kang, Yingli, Lu, Hua, Niu, Honglin, Liu, Wei, Li, Ying
• Format: Journal Article
• Language: English
• Published: United States Wiley Subscription Services, Inc 01.04.2019
• Subjects: Animal models; Animals; Antioxidants; Apoptosis; Apoptosis - drug effects; Attenuation; Biosynthesis; Cell Line; Cytoplasm; Diabetes; Diabetes mellitus; Diabetes Mellitus, Experimental - pathology; Diabetic nephropathy; DIABLO protein; Disease Models, Animal; Electron transport chain; Epithelial cells; Glucose; Glucose - metabolism; In vivo methods and tests; Male; Malondialdehyde; Malondialdehyde - metabolism; Membrane potential; Membrane Potential, Mitochondrial - drug effects; Mice; Mitochondria; Mitochondria - metabolism; Nephropathy; Oxidative stress; Oxidative Stress - physiology; peroxisome proliferator activated; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - metabolism; Podocytes - pathology; Proteinuria; Proteinuria - prevention & control; Reactive oxygen species; Reactive Oxygen Species - metabolism; receptor γ coactivator 1α; Renal cortex; Resveratrol; Resveratrol - pharmacology; SIRT1 protein; Sirtuin 1 - metabolism; Superoxide dismutase; Transcription factors; apoptosis; receptor γ coactivator 1α; resveratrol; diabetic nephropathy; oxidative stress; peroxisome proliferator activated

Excessive generation of mitochondrial reactive oxygen species (ROS) is considered to be initiating event in the development of diabetic nephropathy (DN). Mitochondrial biosynthesis mediated by coactivator PGC‐1α and its downstream transcription factors NRF1 and TFAM may be a key target in maintainin...