Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1016/j.yjmcc.2015.11.010 http://scihub22266oqcxt.onion/10.1016/j.yjmcc.2015.11.010 C4846493!4846493!26562414     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Mol+Cell+Cardiol 2016 ; 93 (ä): 162-74 Nephropedia Template TP {{tp|p=26562414|t=2016. Integrins and Integrin-related Proteins in Cardiac Fibrosis |pdf=|usr=}}{{26562414}} gab.com Text Integrins and Integrin-related Proteins in Cardiac Fibrosis JO: J Mol Cell Cardiol http://www.kidney.de/pget.php?&tw=1&pmid=26562414 #FOAvip Cardiac fibrosis is one of the major components of the healing mechanism following any injury of the heart and as such may contribute to both systolic and diastolic dysfunction in a range of pathophysiologic conditions. Canonically, it can occur as part of the remodeling process that occurs following myocardial infarction or that follows as a response to pressure overload. Integrins are cell surface receptors which act in both cellular adhesion and signaling. Most importantly, in the context of the continuously contracting myocardium, they are recognized as mechanotransducers. They have been implicated in the development of fibrosis in several organs, including the heart. This review will focus on the involvement of integrins and integrin-related proteins, in cardiac fibrosis, outlining the roles of these proteins in the fibrotic responses in specific cardiac pathologies, discuss some of the common end effectors (Angiotensin II, transforming growth factor beta 1 and mechanical stress) through which integrins function and finally discuss how manipulation of this set of proteins may lead to new treatments which could prove useful to alter the deleterious effects of cardiac fibrosis. Twit Text FOAVip Integrins and Integrin-related Proteins in Cardiac Fibrosis ????J Mol Cell Cardiol http://www.kidney.de/pget.php?&tw=1&pmid=26562414 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26562414 #FOAvip English Wikipedia <ref>{{Cite pmid|26562414}}</ref> Integrins and Integrin-related Proteins in Cardiac Fibrosis #MMPMID26562414 Chen C; Li R; Ross RS; Manso AM J Mol Cell Cardiol 2016[Apr]; 93 (ä): 162-74 PMID26562414show ga Cardiac fibrosis is one of the major components of the healing mechanism following any injury of the heart and as such may contribute to both systolic and diastolic dysfunction in a range of pathophysiologic conditions. Canonically, it can occur as part of the remodeling process that occurs following myocardial infarction or that follows as a response to pressure overload. Integrins are cell surface receptors which act in both cellular adhesion and signaling. Most importantly, in the context of the continuously contracting myocardium, they are recognized as mechanotransducers. They have been implicated in the development of fibrosis in several organs, including the heart. This review will focus on the involvement of integrins and integrin-related proteins, in cardiac fibrosis, outlining the roles of these proteins in the fibrotic responses in specific cardiac pathologies, discuss some of the common end effectors (Angiotensin II, transforming growth factor beta 1 and mechanical stress) through which integrins function and finally discuss how manipulation of this set of proteins may lead to new treatments which could prove useful to alter the deleterious effects of cardiac fibrosis. äIntegrins and Integrin-related Proteins in Cardiac Fibrosis (epmc).pdf DeepDyve Pubget Overpricing