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10.1002/hep.27376 http://scihub22266oqcxt.onion/10.1002/hep.27376 C4333127!4333127!25131509     free     free     free       Hepatology 2015 ; 61 (5): 1740-6 Nephropedia Template TP {{tp|p=25131509|t=2015. Liver Sinusoidal Endothelial Cells in Hepatic Fibrosis |pdf=|usr=}}{{25131509}} gab.com Text Liver Sinusoidal Endothelial Cells in Hepatic Fibrosis JO: Hepatology http://www.kidney.de/pget.php?&tw=1&pmid=25131509 #FOAvip Capillarization, lack of liver sinusoidal endothelial cell (LSEC) fenestration and formation of an organized basement membrane, not only precedes fibrosis, but is also permissive for hepatic stellate cell activation and fibrosis. Thus dysregulation of the LSEC phenotype is a critical step in the fibrotic process. Both a VEGF-stimulated, NO-independent pathway and a VEGF-stimulated NO-dependent pathway are necessary to maintain the differentiated LSEC phenotype. The NO-dependent pathway is impaired in capillarization and activation of this pathway downstream from NO restores LSEC differentiation in vivo. Restoration of LSEC differentiation in vivo promotes HSC quiescence, enhances regression of fibrosis, and prevents progression of cirrhosis. Twit Text FOAVip Liver Sinusoidal Endothelial Cells in Hepatic Fibrosis ????Hepatology http://www.kidney.de/pget.php?&tw=1&pmid=25131509 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25131509 #FOAvip English Wikipedia <ref>{{Cite pmid|25131509}}</ref> Liver Sinusoidal Endothelial Cells in Hepatic Fibrosis #MMPMID25131509 DeLeve LD Hepatology 2015[May]; 61 (5): 1740-6 PMID25131509show ga Capillarization, lack of liver sinusoidal endothelial cell (LSEC) fenestration and formation of an organized basement membrane, not only precedes fibrosis, but is also permissive for hepatic stellate cell activation and fibrosis. Thus dysregulation of the LSEC phenotype is a critical step in the fibrotic process. Both a VEGF-stimulated, NO-independent pathway and a VEGF-stimulated NO-dependent pathway are necessary to maintain the differentiated LSEC phenotype. The NO-dependent pathway is impaired in capillarization and activation of this pathway downstream from NO restores LSEC differentiation in vivo. Restoration of LSEC differentiation in vivo promotes HSC quiescence, enhances regression of fibrosis, and prevents progression of cirrhosis. äLiver Sinusoidal Endothelial Cells in Hepatic Fibrosis (epmc).pdf DeepDyve Pubget Overpricing