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10.1242/jcs.162891 http://scihub22266oqcxt.onion/10.1242/jcs.162891 C4457157!4457157!25918124     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 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Cell+Sci 2015 ; 128 (10): 1865-75 Nephropedia Template TP {{tp|p=25918124|t=2015. Mechanobiology of myofibroblast adhesion in fibrotic cardiac disease |pdf=|usr=}}{{25918124}} gab.com Text Mechanobiology of myofibroblast adhesion in fibrotic cardiac disease JO: J Cell Sci http://www.kidney.de/pget.php?&tw=1&pmid=25918124 #FOAvip Fibrotic cardiac disease, a leading cause of death worldwide, manifests as substantial loss of function following maladaptive tissue remodeling. Fibrosis can affect both the heart valves and the myocardium and is characterized by the activation of fibroblasts and accumulation of extracellular matrix. Valvular interstitial cells and cardiac fibroblasts, the cell types responsible for maintenance of cardiac extracellular matrix, are sensitive to changing mechanical environments, and their ability to sense and respond to mechanical forces determines both normal development and the progression of disease. Recent studies have uncovered specific adhesion proteins and mechano-sensitive signaling pathways that contribute to the progression of fibrosis. Integrins form adhesions with the extracellular matrix, and respond to changes in substrate stiffness and extracellular matrix composition. Cadherins mechanically link neighboring cells and are likely to contribute to fibrotic disease propagation. Finally, transition to the active myofibroblast phenotype leads to maladaptive tissue remodeling and enhanced mechanotransductive signaling, forming a positive feedback loop that contributes to heart failure. This Commentary summarizes recent findings on the role of mechanotransduction through integrins and cadherins to perpetuate mechanically induced differentiation and fibrosis in the context of cardiac disease. Twit Text FOAVip Mechanobiology of myofibroblast adhesion in fibrotic cardiac disease ????J Cell Sci http://www.kidney.de/pget.php?&tw=1&pmid=25918124 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25918124 #FOAvip English Wikipedia <ref>{{Cite pmid|25918124}}</ref> Mechanobiology of myofibroblast adhesion in fibrotic cardiac disease #MMPMID25918124 Schroer AK; Merryman WD J Cell Sci 2015[May]; 128 (10): 1865-75 PMID25918124show ga Fibrotic cardiac disease, a leading cause of death worldwide, manifests as substantial loss of function following maladaptive tissue remodeling. Fibrosis can affect both the heart valves and the myocardium and is characterized by the activation of fibroblasts and accumulation of extracellular matrix. Valvular interstitial cells and cardiac fibroblasts, the cell types responsible for maintenance of cardiac extracellular matrix, are sensitive to changing mechanical environments, and their ability to sense and respond to mechanical forces determines both normal development and the progression of disease. Recent studies have uncovered specific adhesion proteins and mechano-sensitive signaling pathways that contribute to the progression of fibrosis. Integrins form adhesions with the extracellular matrix, and respond to changes in substrate stiffness and extracellular matrix composition. Cadherins mechanically link neighboring cells and are likely to contribute to fibrotic disease propagation. Finally, transition to the active myofibroblast phenotype leads to maladaptive tissue remodeling and enhanced mechanotransductive signaling, forming a positive feedback loop that contributes to heart failure. This Commentary summarizes recent findings on the role of mechanotransduction through integrins and cadherins to perpetuate mechanically induced differentiation and fibrosis in the context of cardiac disease. äMechanobiology of myofibroblast adhesion in fibrotic cardiac disease (epmc).pdf DeepDyve Pubget Overpricing