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10.1016/j.yjmcc.2016.02.011 http://scihub22266oqcxt.onion/10.1016/j.yjmcc.2016.02.011 C4987078!4987078!26876451     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26876451&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       J+Mol+Cell+Cardiol 2016 ; 92 (ä): 206-13 Nephropedia Template TP {{tp|p=26876451|t=2016. Epigenetic regulation of cardiac fibrosis |pdf=|usr=}}{{26876451}} gab.com Text Epigenetic regulation of cardiac fibrosis JO: J Mol Cell Cardiol http://www.kidney.de/pget.php?&tw=1&pmid=26876451 #FOAvip Fibrosis is defined as excess deposition of extracellular matrix (ECM), resulting in tissue scarring and organ dysfunction. In the heart, fibrosis may be reparative, replacing areas of myocyte loss with a structural scar following infarction, or reactive, which is triggered in the absence of cell death and involves interstitial ECM deposition in response to long-lasting stress. Interstitial fibrosis can increase the passive stiffness of the myocardium, resulting in impaired relaxation and diastolic dysfunction. Additionally, fibrosis can lead to disruption of electrical conduction in the heart, causing arrhythmias, and can limit myocyte oxygen availability and thus exacerbate myocardial ischemia. Here, we review recent studies that have illustrated key roles for epigenetic events in the control of pro-fibrotic gene expression, and highlight the potential of small molecules that target epigenetic regulators as a means of treating fibrotic cardiac diseases. Twit Text FOAVip Epigenetic regulation of cardiac fibrosis ????J Mol Cell Cardiol http://www.kidney.de/pget.php?&tw=1&pmid=26876451 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26876451 #FOAvip English Wikipedia <ref>{{Cite pmid|26876451}}</ref> Epigenetic regulation of cardiac fibrosis #MMPMID26876451 Stratton MS; McKinsey TA J Mol Cell Cardiol 2016[Mar]; 92 (ä): 206-13 PMID26876451show ga Fibrosis is defined as excess deposition of extracellular matrix (ECM), resulting in tissue scarring and organ dysfunction. In the heart, fibrosis may be reparative, replacing areas of myocyte loss with a structural scar following infarction, or reactive, which is triggered in the absence of cell death and involves interstitial ECM deposition in response to long-lasting stress. Interstitial fibrosis can increase the passive stiffness of the myocardium, resulting in impaired relaxation and diastolic dysfunction. Additionally, fibrosis can lead to disruption of electrical conduction in the heart, causing arrhythmias, and can limit myocyte oxygen availability and thus exacerbate myocardial ischemia. Here, we review recent studies that have illustrated key roles for epigenetic events in the control of pro-fibrotic gene expression, and highlight the potential of small molecules that target epigenetic regulators as a means of treating fibrotic cardiac diseases. äEpigenetic regulation of cardiac fibrosis (epmc).pdf DeepDyve Pubget Overpricing