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10.1016/j.bbadis.2016.01.011 http://scihub22266oqcxt.onion/10.1016/j.bbadis.2016.01.011 C4791054!4791054!26775029     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Biochim+Biophys+Acta 2016 ; 1862 (4): 763-77 Nephropedia Template TP {{tp|p=26775029|t=2016. Chronic heart failure: Ca2+, catabolism, and catastrophic cell death |pdf=|usr=}}{{26775029}} gab.com Text Chronic heart failure: Ca2+, catabolism, and catastrophic cell death JO: Biochim Biophys Acta http://www.kidney.de/pget.php?&tw=1&pmid=26775029 #FOAvip Robust successes have been achieved in recent years in conquering the acutely lethal manifestations of heart disease. Many patients who previously would have died now survive to enjoy happy and productive lives. Nevertheless, the devastating impact of heart disease continues unabated, as the spectrum of disease has evolved with new manifestations. In light of this ever-evolving challenge, insights that culminate in novel therapeutic targets are urgently needed. Here, we review fundamental mechanisms of heart failure, both with reduced (HFrEF) and preserved (HFpEF) ejection fraction. We discuss pathways that regulate cardiomyocyte remodeling and turnover, focusing on Ca2+ signaling, autophagy, and apoptosis. In particular, we highlight recent insights pointing to novel connections among these events. We also explore mechanisms whereby potential therapeutic approaches targeting these processes may improve morbidity and mortality in the devastating syndrome of heart failure. Twit Text FOAVip Chronic heart failure: Ca2+, catabolism, and catastrophic cell death ????Biochim Biophys Acta http://www.kidney.de/pget.php?&tw=1&pmid=26775029 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26775029 #FOAvip English Wikipedia <ref>{{Cite pmid|26775029}}</ref> Chronic heart failure: Ca2+, catabolism, and catastrophic cell death #MMPMID26775029 Cho GW; Altamirano F; Hill JA Biochim Biophys Acta 2016[Apr]; 1862 (4): 763-77 PMID26775029show ga Robust successes have been achieved in recent years in conquering the acutely lethal manifestations of heart disease. Many patients who previously would have died now survive to enjoy happy and productive lives. Nevertheless, the devastating impact of heart disease continues unabated, as the spectrum of disease has evolved with new manifestations. In light of this ever-evolving challenge, insights that culminate in novel therapeutic targets are urgently needed. Here, we review fundamental mechanisms of heart failure, both with reduced (HFrEF) and preserved (HFpEF) ejection fraction. We discuss pathways that regulate cardiomyocyte remodeling and turnover, focusing on Ca2+ signaling, autophagy, and apoptosis. In particular, we highlight recent insights pointing to novel connections among these events. We also explore mechanisms whereby potential therapeutic approaches targeting these processes may improve morbidity and mortality in the devastating syndrome of heart failure. äChronic heart failure: Ca2+, catabolism, and catastrophic cell death (epmc).pdf DeepDyve Pubget Overpricing