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10.18632/oncotarget.17165 http://scihub22266oqcxt.onion/10.18632/oncotarget.17165 C5503635!5503635!28465484     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       Oncotarget 2017 ; 8 (24): 39592-604 Nephropedia Template TP {{tp|p=28465484|t=2017. SIRT3-KLF15 signaling ameliorates kidney injury induced by hypertension |pdf=|usr=}}{{28465484}} gab.com Text SIRT3-KLF15 signaling ameliorates kidney injury induced by hypertension JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=28465484 #FOAvip Renal fibrosis participates in the progression of hypertension-induced kidney injury. The effect of SIRT3, a member of the NAD+-dependent deacetylase family, in hypertensive nephropathy remains unclear. In this study, we found that SIRT3 was reduced after angiotensin II (AngII) treatment both in vivo and in vitro. Furthermore, SIRT3-knockout mice aggravated hypertension-induced renal dysfunction and renal fibrosis via chronic AngII infusion (2000 ng/kg per minute for 42 days). On the contrary, SIRT3-overexpression mice attenuated AngII-induced kidney injury compared with wild-type mice. Remarkably, a co-localization of SIRT3 and KLF15, a kidney-enriched nuclear transcription factor, led to SIRT3 directly deacetylating KLF15, followed by decreased expression of fibronectin and collagen type IV in cultured MPC-5 podocytes. In addition, honokiol (HKL), a major bioactive compound isolated from Magnolia officinalis (Houpo), suppressed AngII-induced renal fibrosis through activating SIRT3-KLF15 signaling. Taken together, our findings implicate that a novel SIRT3-KLF15 signaling may prevent kidney injury from hypertension and HKL can act as a SIRT3-KLF15 signaling activator to protect against hypertensive nephropathy. Twit Text FOAVip SIRT3-KLF15 signaling ameliorates kidney injury induced by hypertension ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=28465484 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28465484 #FOAvip English Wikipedia <ref>{{Cite pmid|28465484}}</ref> SIRT3-KLF15 signaling ameliorates kidney injury induced by hypertension #MMPMID28465484 Li N; Zhang J; Yan X; Zhang C; Liu H; Shan X; Li J; Yang Y; Huang C; Zhang P; Zhang Y; Bu P Oncotarget 2017[Jun]; 8 (24): 39592-604 PMID28465484show ga Renal fibrosis participates in the progression of hypertension-induced kidney injury. The effect of SIRT3, a member of the NAD+-dependent deacetylase family, in hypertensive nephropathy remains unclear. In this study, we found that SIRT3 was reduced after angiotensin II (AngII) treatment both in vivo and in vitro. Furthermore, SIRT3-knockout mice aggravated hypertension-induced renal dysfunction and renal fibrosis via chronic AngII infusion (2000 ng/kg per minute for 42 days). On the contrary, SIRT3-overexpression mice attenuated AngII-induced kidney injury compared with wild-type mice. Remarkably, a co-localization of SIRT3 and KLF15, a kidney-enriched nuclear transcription factor, led to SIRT3 directly deacetylating KLF15, followed by decreased expression of fibronectin and collagen type IV in cultured MPC-5 podocytes. In addition, honokiol (HKL), a major bioactive compound isolated from Magnolia officinalis (Houpo), suppressed AngII-induced renal fibrosis through activating SIRT3-KLF15 signaling. Taken together, our findings implicate that a novel SIRT3-KLF15 signaling may prevent kidney injury from hypertension and HKL can act as a SIRT3-KLF15 signaling activator to protect against hypertensive nephropathy. äSIRT3-KLF15 signaling ameliorates kidney injury induced by hypertensio(epmc).pdf DeepDyve Pubget Overpricing