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10.21037/atm.2016.10.33 http://scihub22266oqcxt.onion/10.21037/atm.2016.10.33 C5107387!5107387!27867963     free     free     free Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Ann+Transl+Med 2016 ; 4 (20): ä Nephropedia Template TP {{tp|p=27867963|t=2016. ?v?1 integrin as a novel therapeutic target for tissue fibrosis |pdf=|usr=}}{{27867963}} gab.com Text v 1 integrin as a novel therapeutic target for tissue fibrosis JO: Ann Transl Med http://www.kidney.de/pget.php?&tw=1&pmid=27867963 #FOAvip Chronic tissue injury with fibrosis results in disruption of tissue architecture, organ dysfunction and eventually organ failure. Currently, therapeutic options for tissue fibrosis are severely limited and organ transplantation including high cost and co-morbidities is the only effective treatment for end-stage fibrotic disease. Therefore, it is imperative to develop effective anti-fibrotic agents. Integrins are transmembrane proteins and are major receptors for cell-extracellular matrix (ECM) and cell-cell adhesion. Modulation of these molecules, particularly ?v integrin family, has exhibited profound effects on fibrosis in multiple organ and disease state. Based on the several studies, the integrins ?v?3, ?v?5, ?v?6, and ?v?8 have been known to modulate the fibrotic process via activation of latent transforming growth factor (TGF)-? in pre-clinical models of fibrosis. In this perspective, we reviewed the functions of ?v?1 integrin as a potentially useful target molecule for antifibrotic agent and introduced novel specific small-molecule inhibitors targeting this integrin. Twit Text FOAVip v 1 integrin as a novel therapeutic target for tissue fibrosis ????Ann Transl Med http://www.kidney.de/pget.php?&tw=1&pmid=27867963 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27867963 #FOAvip English Wikipedia <ref>{{Cite pmid|27867963}}</ref> ?v?1 integrin as a novel therapeutic target for tissue fibrosis #MMPMID27867963 Song KH; Cho SJ; Song JY Ann Transl Med 2016[Oct]; 4 (20): ä PMID27867963show ga Chronic tissue injury with fibrosis results in disruption of tissue architecture, organ dysfunction and eventually organ failure. Currently, therapeutic options for tissue fibrosis are severely limited and organ transplantation including high cost and co-morbidities is the only effective treatment for end-stage fibrotic disease. Therefore, it is imperative to develop effective anti-fibrotic agents. Integrins are transmembrane proteins and are major receptors for cell-extracellular matrix (ECM) and cell-cell adhesion. Modulation of these molecules, particularly ?v integrin family, has exhibited profound effects on fibrosis in multiple organ and disease state. Based on the several studies, the integrins ?v?3, ?v?5, ?v?6, and ?v?8 have been known to modulate the fibrotic process via activation of latent transforming growth factor (TGF)-? in pre-clinical models of fibrosis. In this perspective, we reviewed the functions of ?v?1 integrin as a potentially useful target molecule for antifibrotic agent and introduced novel specific small-molecule inhibitors targeting this integrin. ä?v?1 integrin as a novel therapeutic target for tissue fibrosis (epmc).pdf DeepDyve Pubget Overpricing