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10.1038/nrcardio.2016.203 http://scihub22266oqcxt.onion/10.1038/nrcardio.2016.203 C5350035!5350035!28004807     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28004807&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Rev+Cardiol 2017 ; 14 (4): 238-50 Nephropedia Template TP {{tp|p=28004807|t=2017. Mitochondrial function as a therapeutic target in heart failure |pdf=|usr=}}{{28004807}} gab.com Text Mitochondrial function as a therapeutic target in heart failure JO: Nat Rev Cardiol http://www.kidney.de/pget.php?&tw=1&pmid=28004807 #FOAvip Heart failure is a pressing worldwide public-health problem with millions of patients having worsening heart failure. Despite all the available therapies, the condition carries a very poor prognosis. Existing therapies provide symptomatic and clinical benefit, but do not fully address molecular abnormalities that occur in cardiomyocytes. This shortcoming is particularly important given that most patients with heart failure have viable dysfunctional myocardium, in which an improvement or normalization of function might be possible. Although the pathophysiology of heart failure is complex, mitochondrial dysfunction seems to be an important target for therapy to improve cardiac function directly. Mitochondrial abnormalities include impaired mitochondrial electron transport chain activity, increased formation of reactive oxygen species, shifted metabolic substrate utilization, aberrant mitochondrial dynamics, and altered ion homeostasis. In this Consensus Statement, insights into the mechanisms of mitochondrial dysfunction in heart failure are presented, along with an overview of emerging treatments with the potential to improve the function of the failing heart by targeting mitochondria. Twit Text FOAVip Mitochondrial function as a therapeutic target in heart failure ????Nat Rev Cardiol http://www.kidney.de/pget.php?&tw=1&pmid=28004807 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28004807 #FOAvip English Wikipedia <ref>{{Cite pmid|28004807}}</ref> Mitochondrial function as a therapeutic target in heart failure #MMPMID28004807 Brown DA; Perry JB; Allen ME; Sabbah HN; Stauffer BL; Shaikh SR; Cleland JGF; Colucci WS; Butler J; Voors AA; Anker SD; Pitt B; Pieske B; Filippatos G; Greene SJ; Gheorghiade M Nat Rev Cardiol 2017[Apr]; 14 (4): 238-50 PMID28004807show ga Heart failure is a pressing worldwide public-health problem with millions of patients having worsening heart failure. Despite all the available therapies, the condition carries a very poor prognosis. Existing therapies provide symptomatic and clinical benefit, but do not fully address molecular abnormalities that occur in cardiomyocytes. This shortcoming is particularly important given that most patients with heart failure have viable dysfunctional myocardium, in which an improvement or normalization of function might be possible. Although the pathophysiology of heart failure is complex, mitochondrial dysfunction seems to be an important target for therapy to improve cardiac function directly. Mitochondrial abnormalities include impaired mitochondrial electron transport chain activity, increased formation of reactive oxygen species, shifted metabolic substrate utilization, aberrant mitochondrial dynamics, and altered ion homeostasis. In this Consensus Statement, insights into the mechanisms of mitochondrial dysfunction in heart failure are presented, along with an overview of emerging treatments with the potential to improve the function of the failing heart by targeting mitochondria. äMitochondrial function as a therapeutic target in heart failure (epmc).pdf DeepDyve Pubget Overpricing