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10.1159/000368932 http://scihub22266oqcxt.onion/10.1159/000368932 C4458239!4458239!25503637     free     free     free Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\25503637.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Nephron+Exp+Nephrol ä ; ä (ä): ä Nephropedia Template TP {{tp|p=25503637|t=ä. Beneficial Effects of AMPK Agonists in Kidney Ischemia Reperfusion: Autophagy and Cellular Stress Markers |pdf=|usr=}}{{25503637}} gab.com Text Beneficial Effects of AMPK Agonists in Kidney Ischemia Reperfusion: Autophagy and Cellular Stress Markers JO: Nephron Exp Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=25503637 #FOAvip Background: Kidney ischemia-reperfusion is a form of acute kidney injury resulting in a cascade of cellular events prompting rapid cellular damage and suppression of kidney function. A cellular response to ischemic stress is the activation of AMP-activated protein kinase (AMPK) where AMPK induces a number of homeostatic and renoprotective mechanisms, including autophagy. However whether autophagy is beneficial or detrimental in ischemia-reperfusion remains controversial. We investigated the effects of agonist induction of AMPK activity on autophagy and cell stress proteins in the model of kidney ischemia-reperfusion. Methods: AMPK agonists, AICAR (0.1g/kg) and Metformin (0.3g/kg), were administered 24 hours prior to ischemia, with kidneys harvested at 24 hours of reperfusion. Results: We observed a paradoxical decrease in AMPK activity accompanied by increases in mTORC1 activity and p62/SQSTM1 expression. These results lead us to propose that AMPK and autophagy was insufficient to properly counter the cellular insults in ischemia-reperfusion. Agonist induction of AMPK activity with AICAR or metformin increased macroautophagy protein LC3 and normalizes p62/SQSTM1 expression and mTOR activity. Ischemia-reperfusion increases in Beclin-1 and PINK1 expressions, consistent with increased mitophagy, were also mitigated with AMPK agonists. Stress responsive and apoptotic marker expressions increase in ischemia-reperfusion and are significantly attenuated with agonist administration, as are early indicators of fibrosis. Conclusions: Our data suggest that levels of renoprotective AMPK activity and canonical autophagy are insufficient to maintain cellular homeostasis contributing to the progression of ischemia-reperfusion injury. We further demonstrate that induction of AMPK activity can provide beneficial cellular effects in containing injury in ischemia-reperfusion. Twit Text FOAVip Beneficial Effects of AMPK Agonists in Kidney Ischemia Reperfusion: Autophagy and Cellular Stress Markers ????Nephron Exp Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=25503637 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25503637 #FOAvip English Wikipedia <ref>{{Cite pmid|25503637}}</ref> Beneficial Effects of AMPK Agonists in Kidney Ischemia Reperfusion: Autophagy and Cellular Stress Markers #MMPMID25503637 Declèves AE; Sharma K; Satriano J Nephron Exp Nephrol ä[]; ä (ä): ä PMID25503637show ga Background: Kidney ischemia-reperfusion is a form of acute kidney injury resulting in a cascade of cellular events prompting rapid cellular damage and suppression of kidney function. A cellular response to ischemic stress is the activation of AMP-activated protein kinase (AMPK) where AMPK induces a number of homeostatic and renoprotective mechanisms, including autophagy. However whether autophagy is beneficial or detrimental in ischemia-reperfusion remains controversial. We investigated the effects of agonist induction of AMPK activity on autophagy and cell stress proteins in the model of kidney ischemia-reperfusion. Methods: AMPK agonists, AICAR (0.1g/kg) and Metformin (0.3g/kg), were administered 24 hours prior to ischemia, with kidneys harvested at 24 hours of reperfusion. Results: We observed a paradoxical decrease in AMPK activity accompanied by increases in mTORC1 activity and p62/SQSTM1 expression. These results lead us to propose that AMPK and autophagy was insufficient to properly counter the cellular insults in ischemia-reperfusion. Agonist induction of AMPK activity with AICAR or metformin increased macroautophagy protein LC3 and normalizes p62/SQSTM1 expression and mTOR activity. Ischemia-reperfusion increases in Beclin-1 and PINK1 expressions, consistent with increased mitophagy, were also mitigated with AMPK agonists. Stress responsive and apoptotic marker expressions increase in ischemia-reperfusion and are significantly attenuated with agonist administration, as are early indicators of fibrosis. Conclusions: Our data suggest that levels of renoprotective AMPK activity and canonical autophagy are insufficient to maintain cellular homeostasis contributing to the progression of ischemia-reperfusion injury. We further demonstrate that induction of AMPK activity can provide beneficial cellular effects in containing injury in ischemia-reperfusion. äBeneficial Effects of AMPK Agonists in Kidney Ischemia Reperfusion: Au(epmc).pdf DeepDyve Pubget Overpricing