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10.1371/journal.pone.0125176 http://scihub22266oqcxt.onion/10.1371/journal.pone.0125176 C4390193!4390193!25853493     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25853493&cmd=llinks): Failed to open stream: HTTP request failed! 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Protective Role of PGC-1? in Diabetic Nephropathy Is Associated with the Inhibition of ROS through Mitochondrial Dynamic Remodeling |pdf=|usr=}}{{25853493}} gab.com Text Protective Role of PGC-1 in Diabetic Nephropathy Is Associated with the Inhibition of ROS through Mitochondrial Dynamic Remodeling JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=25853493 #FOAvip The overproduction of mitochondrial reactive oxygen species (ROS) plays a key role in the pathogenesis of diabetic nephropathy (DN). However, the underlying molecular mechanism remains unclear. Our aim was to investigate the role of PGC-1? in the pathogenesis of DN. Rat glomerular mesangial cells (RMCs) were incubated in normal or high glucose medium with or without the PGC-1?-overexpressing plasmid (pcDNA3-PGC-1?) for 48 h. In the diabetic rats, decreased PGC-1? expression was associated with increased mitochondrial ROS generation in the renal cortex, increased proteinuria, glomerular hypertrophy, and higher glomerular 8-OHdG (a biomarker for oxidative stress). In vitro, hyperglycemia induced the downregulation of PGC-1?, which led to increased DRP1 expression, increased mitochondrial fragmentation and damaged network structure. This was associated with an increase in ROS generation and mesangial cell hypertrophy. These pathological changes were reversed in vitro by the transfection of pcDNA3-PGC-1?. These data suggest that PGC-1? may protect DN via the inhibition of DRP1-mediated mitochondrial dynamic remodeling and ROS production. These findings may assist the development of novel therapeutic strategies for patients with DN. Twit Text FOAVip Protective Role of PGC-1 in Diabetic Nephropathy Is Associated with the Inhibition of ROS through Mitochondrial Dynamic Remodeling ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=25853493 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25853493 #FOAvip English Wikipedia <ref>{{Cite pmid|25853493}}</ref> Protective Role of PGC-1? in Diabetic Nephropathy Is Associated with the Inhibition of ROS through Mitochondrial Dynamic Remodeling #MMPMID25853493 Guo K; Lu J; Huang Y; Wu M; Zhang L; Yu H; Zhang M; Bao Y; He JC; Chen H; Jia W PLoS One 2015[]; 10 (4): � PMID25853493show ga The overproduction of mitochondrial reactive oxygen species (ROS) plays a key role in the pathogenesis of diabetic nephropathy (DN). However, the underlying molecular mechanism remains unclear. Our aim was to investigate the role of PGC-1? in the pathogenesis of DN. Rat glomerular mesangial cells (RMCs) were incubated in normal or high glucose medium with or without the PGC-1?-overexpressing plasmid (pcDNA3-PGC-1?) for 48 h. In the diabetic rats, decreased PGC-1? expression was associated with increased mitochondrial ROS generation in the renal cortex, increased proteinuria, glomerular hypertrophy, and higher glomerular 8-OHdG (a biomarker for oxidative stress). In vitro, hyperglycemia induced the downregulation of PGC-1?, which led to increased DRP1 expression, increased mitochondrial fragmentation and damaged network structure. This was associated with an increase in ROS generation and mesangial cell hypertrophy. These pathological changes were reversed in vitro by the transfection of pcDNA3-PGC-1?. These data suggest that PGC-1? may protect DN via the inhibition of DRP1-mediated mitochondrial dynamic remodeling and ROS production. These findings may assist the development of novel therapeutic strategies for patients with DN. �Protective Role of PGC-1? in Diabetic Nephropathy Is Associated with t(epmc).pdf DeepDyve Pubget Overpricing