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10.1186/s40824-016-0060-8 http://scihub22266oqcxt.onion/10.1186/s40824-016-0060-8 C4879750!4879750 !27226899     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27226899 &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 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\27226899 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Biomater+Res 2016 ; 20 (ä): 13 Nephropedia Template TP {{tp|p=27226899 |t=2016. Antifibrotic therapies to control cardiac fibrosis |pdf=|usr=}}{{27226899 }} gab.com Text Antifibrotic therapies to control cardiac fibrosis JO: Biomater Res http://www.kidney.de/pget.php?&tw=1&pmid=27226899 #FOAvip Cardiac fibrosis occurs naturally after myocardial infarction. While the initially formed fibrotic tissue prevents the infarcted heart tissue from rupture, the progression of cardiac fibrosis continuously expands the size of fibrotic tissue and causes cardiac function decrease. Cardiac fibrosis eventually evolves the infarcted hearts into heart failure. Inhibiting cardiac fibrosis from progressing is critical to prevent heart failure. However, there is no efficient therapeutic approach currently available. Myofibroblasts are primarily responsible for cardiac fibrosis. They are formed by cardiac fibroblast differentiation, fibrocyte differentiation, epithelial to mesenchymal transdifferentiation, and endothelial to mesenchymal transition, driven by cytokines such as transforming growth factor beta (TGF-?), angiotensin II and platelet-derived growth factor (PDGF). The approaches that inhibit myofibroblast formation have been demonstrated to prevent cardiac fibrosis, including systemic delivery of antifibrotic drugs, localized delivery of biomaterials, localized delivery of biomaterials and antifibrotic drugs, and localized delivery of cells using biomaterials. This review addresses current progresses in cardiac fibrosis therapies. Twit Text FOAVip Antifibrotic therapies to control cardiac fibrosis ????Biomater Res http://www.kidney.de/pget.php?&tw=1&pmid=27226899 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27226899 #FOAvip English Wikipedia <ref>{{Cite pmid|27226899 }}</ref> Antifibrotic therapies to control cardiac fibrosis #MMPMID27226899 Fan Z ; Guan J Biomater Res 2016[]; 20 (ä): 13 PMID27226899 show ga Cardiac fibrosis occurs naturally after myocardial infarction. While the initially formed fibrotic tissue prevents the infarcted heart tissue from rupture, the progression of cardiac fibrosis continuously expands the size of fibrotic tissue and causes cardiac function decrease. Cardiac fibrosis eventually evolves the infarcted hearts into heart failure. Inhibiting cardiac fibrosis from progressing is critical to prevent heart failure. However, there is no efficient therapeutic approach currently available. Myofibroblasts are primarily responsible for cardiac fibrosis. They are formed by cardiac fibroblast differentiation, fibrocyte differentiation, epithelial to mesenchymal transdifferentiation, and endothelial to mesenchymal transition, driven by cytokines such as transforming growth factor beta (TGF-?), angiotensin II and platelet-derived growth factor (PDGF). The approaches that inhibit myofibroblast formation have been demonstrated to prevent cardiac fibrosis, including systemic delivery of antifibrotic drugs, localized delivery of biomaterials, localized delivery of biomaterials and antifibrotic drugs, and localized delivery of cells using biomaterials. This review addresses current progresses in cardiac fibrosis therapies. äAntifibrotic therapies to control cardiac fibrosis (epmc).pdf DeepDyve Pubget Overpricing