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10.1586/14779072.2016.1147348 http://scihub22266oqcxt.onion/10.1586/14779072.2016.1147348 C4932866!4932866 !26818589     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\26818589 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Expert+Rev+Cardiovasc+Ther 2016 ; 14 (5 ): 591-8 Nephropedia Template TP {{tp|p=26818589 |t=2016. Myofibroblast secretome and its auto-/paracrine signaling |pdf=|usr=}}{{26818589 }} gab.com Text Myofibroblast secretome and its auto-/paracrine signaling JO: Expert Rev Cardiovasc Ther http://www.kidney.de/pget.php?&tw=1&pmid=26818589 #FOAvip Myofibroblasts (myoFb) are phenotypically transformed, contractile fibroblast-like cells expressing ?-smooth muscle actin microfilaments. They are integral to collagen fibrillogenesis with scar tissue formation at sites of repair irrespective of the etiologic origins of injury or tissue involved. MyoFb can persist long after healing is complete, where their ongoing turnover of collagen accounts for a progressive structural remodeling of an organ (a.k.a. fibrosis, sclerosis or cirrhosis). Such persistent metabolic activity is derived from a secretome consisting of requisite components in the de novo generation of angiotensin (Ang) II. Autocrine and paracrine signaling induced by tissue AngII is expressed via AT1 receptor ligand binding to respectively promote: i) regulation of myoFb collagen synthesis via the fibrogenic cytokine TGF-?1-Smad pathway; and ii) dedifferentiation and protein degradation of atrophic myocytes immobilized and ensnared by fibrillar collagen at sites of scarring. Several cardioprotective strategies in the prevention of fibrosis and involving myofibroblasts are considered. They include: inducing myoFb apoptosis through inactivation of antiapoptotic proteins; AT1 receptor antagonist to interfere with auto-/paracrine myoFb signaling or to induce counterregulatory expression of ACE2; and attacking the AngII-AT1R-TGF-?1-Smad pathway by antibody or the use of triplex-forming oligonucleotides. Twit Text FOAVip Myofibroblast secretome and its auto-/paracrine signaling ????Expert Rev Cardiovasc Ther http://www.kidney.de/pget.php?&tw=1&pmid=26818589 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26818589 #FOAvip English Wikipedia <ref>{{Cite pmid|26818589 }}</ref> Myofibroblast secretome and its auto-/paracrine signaling #MMPMID26818589 Bomb R ; Heckle MR ; Sun Y ; Mancarella S ; Guntaka RV ; Gerling IC ; Weber KT Expert Rev Cardiovasc Ther 2016[]; 14 (5 ): 591-8 PMID26818589 show ga Myofibroblasts (myoFb) are phenotypically transformed, contractile fibroblast-like cells expressing ?-smooth muscle actin microfilaments. They are integral to collagen fibrillogenesis with scar tissue formation at sites of repair irrespective of the etiologic origins of injury or tissue involved. MyoFb can persist long after healing is complete, where their ongoing turnover of collagen accounts for a progressive structural remodeling of an organ (a.k.a. fibrosis, sclerosis or cirrhosis). Such persistent metabolic activity is derived from a secretome consisting of requisite components in the de novo generation of angiotensin (Ang) II. Autocrine and paracrine signaling induced by tissue AngII is expressed via AT1 receptor ligand binding to respectively promote: i) regulation of myoFb collagen synthesis via the fibrogenic cytokine TGF-?1-Smad pathway; and ii) dedifferentiation and protein degradation of atrophic myocytes immobilized and ensnared by fibrillar collagen at sites of scarring. Several cardioprotective strategies in the prevention of fibrosis and involving myofibroblasts are considered. They include: inducing myoFb apoptosis through inactivation of antiapoptotic proteins; AT1 receptor antagonist to interfere with auto-/paracrine myoFb signaling or to induce counterregulatory expression of ACE2; and attacking the AngII-AT1R-TGF-?1-Smad pathway by antibody or the use of triplex-forming oligonucleotides. |Angiotensin II/metabolism [MESH] |Collagen/*metabolism [MESH] |Fibroblasts/metabolism [MESH] |Fibrosis/pathology [MESH] |Humans [MESH] |Myofibroblasts/*metabolism [MESH] |Paracrine Communication/*physiology [MESH]Myofibroblast secretome and its auto-/paracrine signaling (epmc).pdf DeepDyve Pubget Overpricing