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10.1161/CIRCRESAHA.116.302317 http://scihub22266oqcxt.onion/10.1161/CIRCRESAHA.116.302317 C4380242!4380242!25814686     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Circ+Res 2015 ; 116 (7): 1254-68 Nephropedia Template TP {{tp|p=25814686|t=2015. INNATE IMMUNITY AND THE FAILING HEART: THE CYTOKINE HYPOTHESIS REVISITED |pdf=|usr=}}{{25814686}} gab.com Text INNATE IMMUNITY AND THE FAILING HEART: THE CYTOKINE HYPOTHESIS REVISITED JO: Circ Res http://www.kidney.de/pget.php?&tw=1&pmid=25814686 #FOAvip Elevated levels of inflammatory mediators have been identified in patients with heart failure, including heart failure with reduced and preserved ejection fraction, as well as acute decompensated heart failure. Moreover, experimental studies have shown repeatedly that activation of inflammation in the heart provokes left ventricular (LV) remodeling and LV dysfunction. Nonetheless, phase III clinical trials that have attempted to antagonize inflammatory mediators have been negative with respect to the primary end points of the trials, and in some patients, resulted in worsening heart failure and/or death. The following review will discuss how recent developments in the field of innate immunity have advanced our understanding of the role of inflammation in the pathogenesis of heart failure and will discuss the negative outcomes of the existing clinical trials in light of this new information. Twit Text FOAVip INNATE IMMUNITY AND THE FAILING HEART: THE CYTOKINE HYPOTHESIS REVISITED ????Circ Res http://www.kidney.de/pget.php?&tw=1&pmid=25814686 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25814686 #FOAvip English Wikipedia <ref>{{Cite pmid|25814686}}</ref> INNATE IMMUNITY AND THE FAILING HEART: THE CYTOKINE HYPOTHESIS REVISITED #MMPMID25814686 Mann DL Circ Res 2015[Mar]; 116 (7): 1254-68 PMID25814686show ga Elevated levels of inflammatory mediators have been identified in patients with heart failure, including heart failure with reduced and preserved ejection fraction, as well as acute decompensated heart failure. Moreover, experimental studies have shown repeatedly that activation of inflammation in the heart provokes left ventricular (LV) remodeling and LV dysfunction. Nonetheless, phase III clinical trials that have attempted to antagonize inflammatory mediators have been negative with respect to the primary end points of the trials, and in some patients, resulted in worsening heart failure and/or death. The following review will discuss how recent developments in the field of innate immunity have advanced our understanding of the role of inflammation in the pathogenesis of heart failure and will discuss the negative outcomes of the existing clinical trials in light of this new information. äINNATE IMMUNITY AND THE FAILING HEART: THE CYTOKINE HYPOTHESIS REVISIT(epmc).pdf DeepDyve Pubget Overpricing