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10.3109/08977194.2011.595714 http://scihub22266oqcxt.onion/10.3109/08977194.2011.595714 C4408550!4408550!21740331     free     free     free       Growth+Factors 2011 ; 29 (5): 196-202 Nephropedia Template TP {{tp|p=21740331|t=2011. TGF-? signaling in fibrosis |pdf=|usr=}}{{21740331}} gab.com Text TGF- signaling in fibrosis JO: Growth Factors http://www.kidney.de/pget.php?&tw=1&pmid=21740331 #FOAvip Transforming growth factor ? (TGF-?) is a central mediator of fibrogenesis. TGF-? is upregulated and activated in fibrotic diseases and modulates fibroblast phenotype and function, inducing myofibroblast transdifferentiation while promoting matrix preservation. Studies in a wide range of experimental models have demonstrated the involvement of the canonical ALK5/Smad3 pathway in fibrosis. Smad-independent pathways may regulate Smad activation and, under certain conditions, may directly transduce fibrogenic signals. The profibrotic actions of TGF-? are mediated, at least in part, through induction of its downstream effector, Connective Tissue Growth Factor. In light of its essential role in the pathogenesis of fibrosis, TGF-? has emerged as an attractive therapeutic target. However, the pleiotropic and multifunctional effects of TGF-? and its role in tissue homeostasis, immunity and cell proliferation raise concerns regarding potential side effects that may be caused by TGF-? blockade. This minireview summarizes the role of TGF-? signaling pathways in the fibrotic response. Twit Text FOAVip TGF- signaling in fibrosis ????Growth Factors http://www.kidney.de/pget.php?&tw=1&pmid=21740331 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=21740331 #FOAvip English Wikipedia <ref>{{Cite pmid|21740331}}</ref> TGF-? signaling in fibrosis #MMPMID21740331 Biernacka A; Dobaczewski M; Frangogiannis NG Growth Factors 2011[Oct]; 29 (5): 196-202 PMID21740331show ga Transforming growth factor ? (TGF-?) is a central mediator of fibrogenesis. TGF-? is upregulated and activated in fibrotic diseases and modulates fibroblast phenotype and function, inducing myofibroblast transdifferentiation while promoting matrix preservation. Studies in a wide range of experimental models have demonstrated the involvement of the canonical ALK5/Smad3 pathway in fibrosis. Smad-independent pathways may regulate Smad activation and, under certain conditions, may directly transduce fibrogenic signals. The profibrotic actions of TGF-? are mediated, at least in part, through induction of its downstream effector, Connective Tissue Growth Factor. In light of its essential role in the pathogenesis of fibrosis, TGF-? has emerged as an attractive therapeutic target. However, the pleiotropic and multifunctional effects of TGF-? and its role in tissue homeostasis, immunity and cell proliferation raise concerns regarding potential side effects that may be caused by TGF-? blockade. This minireview summarizes the role of TGF-? signaling pathways in the fibrotic response. äTGF-? signaling in fibrosis (epmc).pdf DeepDyve Pubget Overpricing