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10.1155/2017/6483572 http://scihub22266oqcxt.onion/10.1155/2017/6483572 C5376939!5376939!28409163     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Diabetes+Res 2017 ; 2017 (ä): ä Nephropedia Template TP {{tp|p=28409163|t=2017. PGC1? Activators Mitigate Diabetic Tubulopathy by Improving Mitochondrial Dynamics and Quality Control |pdf=|usr=}}{{28409163}} gab.com Text PGC1 Activators Mitigate Diabetic Tubulopathy by Improving Mitochondrial Dynamics and Quality Control JO: J Diabetes Res http://www.kidney.de/pget.php?&tw=1&pmid=28409163 #FOAvip Purpose. In this study, we investigated the effect of PGC1? activators on mitochondrial fusion, fission, and autophagic quality control in renal tubular cells in a diabetic environment in vivo and in vitro. We also examined whether the upregulation of PGC1? attenuates diabetic tubulopathy by normalizing mitochondrial homeostasis. Methods. HKC8 cells were subjected to high-glucose conditions (30?mM D-glucose). Diabetes was induced with streptozotocin (STZ, 50?mg/kg i.p. for 5 days) in male C57/BL6J mice. AICAR or metformin was used as a PGC1? activator. Results. Treatment with the PGC1? activators AICAR and metformin improved functional mitochondrial mass in HKC8 cells in high-glucose conditions. Moreover, in renal proximal tubular cells, increased PGC1? activity correlated with the reversal of changes in Drp1, Mfn1, and LC3-II protein expression in a high-glucose environment. Normalized mitochondrial life cycles resulted in low ROS production and reduced apoptosis. AICAR and metformin treatment effectively mitigated albuminuria and renal histopathology and decreased the expression of TGF?1 and ?SMA in the kidneys of diabetic mice. Conclusions. Our results demonstrate that increases in PGC1? activity improve diabetic tubulopathy by modulating mitochondrial dynamics and autophagy. Twit Text FOAVip PGC1 Activators Mitigate Diabetic Tubulopathy by Improving Mitochondrial Dynamics and Quality Control ????J Diabetes Res http://www.kidney.de/pget.php?&tw=1&pmid=28409163 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28409163 #FOAvip English Wikipedia <ref>{{Cite pmid|28409163}}</ref> PGC1? Activators Mitigate Diabetic Tubulopathy by Improving Mitochondrial Dynamics and Quality Control #MMPMID28409163 Lee SY; Kang JM; Kim DJ; Park SH; Jeong HY; Lee YH; Kim YG; Yang DH; Lee SH J Diabetes Res 2017[]; 2017 (ä): ä PMID28409163show ga Purpose. In this study, we investigated the effect of PGC1? activators on mitochondrial fusion, fission, and autophagic quality control in renal tubular cells in a diabetic environment in vivo and in vitro. We also examined whether the upregulation of PGC1? attenuates diabetic tubulopathy by normalizing mitochondrial homeostasis. Methods. HKC8 cells were subjected to high-glucose conditions (30?mM D-glucose). Diabetes was induced with streptozotocin (STZ, 50?mg/kg i.p. for 5 days) in male C57/BL6J mice. AICAR or metformin was used as a PGC1? activator. Results. Treatment with the PGC1? activators AICAR and metformin improved functional mitochondrial mass in HKC8 cells in high-glucose conditions. Moreover, in renal proximal tubular cells, increased PGC1? activity correlated with the reversal of changes in Drp1, Mfn1, and LC3-II protein expression in a high-glucose environment. Normalized mitochondrial life cycles resulted in low ROS production and reduced apoptosis. AICAR and metformin treatment effectively mitigated albuminuria and renal histopathology and decreased the expression of TGF?1 and ?SMA in the kidneys of diabetic mice. Conclusions. Our results demonstrate that increases in PGC1? activity improve diabetic tubulopathy by modulating mitochondrial dynamics and autophagy. äPGC1? Activators Mitigate Diabetic Tubulopathy by Improving Mitochondr(epmc).pdf DeepDyve Pubget Overpricing