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10.3389/fcell.2021.760035 http://scihub22266oqcxt.onion/10.3389/fcell.2021.760035 34778271!8586221!34778271     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Front+Cell+Dev+Biol 2021 ; 9 (ä): 760035 Nephropedia Template TP {{tp|p=34778271|t=2021. Sacubitril Ameliorates Cardiac Fibrosis Through Inhibiting TRPM7 Channel |pdf=|usr=}}{{34778271}} gab.com Text Sacubitril Ameliorates Cardiac Fibrosis Through Inhibiting TRPM7 Channel JO: Front Cell Dev Biol http://www.kidney.de/pget.php?&tw=1&pmid=34778271 #FOAvip Heart failure caused by cardiac fibrosis has become a major challenge of public health worldwide. Cardiomyocyte programmed cell death (PCD) and activation of fibroblasts are crucial pathological features, both of which are associated with aberrant Ca(2+) influx. Transient receptor potential cation channel subfamily M member 7 (TRPM7), the major Ca(2+) permeable channel, plays a regulatory role in cardiac fibrosis. In this study, we sought to explore the mechanistic details for sacubitril, a component of sacubitril/valsartan, in treating cardiac fibrosis. We demonstrated that sacubitril/valsartan could effectively ameliorate cardiac dysfunction and reduce cardiac fibrosis induced by isoprotereno (ISO) in vivo. We further investigated the anti-fibrotic effect of sacubitril in fibroblasts. LBQ657, the metabolite of sacubitril, could significantly attenuate transforming growth factor-beta 1 (TGF-beta1) induced cardiac fibrosis by blocking TRPM7 channel, rather than suppressing its protein expression. In addition, LBQ657 reduced hypoxia-induced cardiomyocyte PCD via suppression of Ca(2+) influx regulated by TRPM7. These findings suggested that sacubitril ameliorated cardiac fibrosis by acting on both fibroblasts and cardiomyocytes through inhibiting TRPM7 channel. Twit Text FOAVip Sacubitril Ameliorates Cardiac Fibrosis Through Inhibiting TRPM7 Channel ????Front Cell Dev Biol http://www.kidney.de/pget.php?&tw=1&pmid=34778271 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34778271 #FOAvip English Wikipedia <ref>{{Cite pmid|34778271}}</ref> Sacubitril Ameliorates Cardiac Fibrosis Through Inhibiting TRPM7 Channel #MMPMID34778271 Jia T; Wang X; Tang Y; Yu W; Li C; Cui S; Zhu J; Meng W; Wang C; Wang Q Front Cell Dev Biol 2021[]; 9 (ä): 760035 PMID34778271show ga Heart failure caused by cardiac fibrosis has become a major challenge of public health worldwide. Cardiomyocyte programmed cell death (PCD) and activation of fibroblasts are crucial pathological features, both of which are associated with aberrant Ca(2+) influx. Transient receptor potential cation channel subfamily M member 7 (TRPM7), the major Ca(2+) permeable channel, plays a regulatory role in cardiac fibrosis. In this study, we sought to explore the mechanistic details for sacubitril, a component of sacubitril/valsartan, in treating cardiac fibrosis. We demonstrated that sacubitril/valsartan could effectively ameliorate cardiac dysfunction and reduce cardiac fibrosis induced by isoprotereno (ISO) in vivo. We further investigated the anti-fibrotic effect of sacubitril in fibroblasts. LBQ657, the metabolite of sacubitril, could significantly attenuate transforming growth factor-beta 1 (TGF-beta1) induced cardiac fibrosis by blocking TRPM7 channel, rather than suppressing its protein expression. In addition, LBQ657 reduced hypoxia-induced cardiomyocyte PCD via suppression of Ca(2+) influx regulated by TRPM7. These findings suggested that sacubitril ameliorated cardiac fibrosis by acting on both fibroblasts and cardiomyocytes through inhibiting TRPM7 channel. äSacubitril Ameliorates Cardiac Fibrosis Through Inhibiting TRPM7 Chann(epmc).pdf DeepDyve Pubget Overpricing