{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T15:06:18Z","timestamp":1792681578960,"version":"4.5.0"},"reference-count":50,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"5","license":[{"start":{"date-parts":[[2015,9,1]],"date-time":"2015-09-01T00:00:00Z","timestamp":1441065600000},"content-version":"tdm","delay-in-days":162,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["Hepatology"],"published-print":{"date-parts":[[2015,5]]},"abstract":"<jats:p>\n                    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 vascular endothelial growth factor (VEGF)\u2010stimulated, nitric oxide (NO)\u2010independent pathway and a VEGF\u2010stimulated NO\u2010dependent pathway are necessary to maintain the differentiated LSEC phenotype. The NO\u2010dependent pathway is impaired in capillarization and activation of this pathway downstream from NO restores LSEC differentiation\n                    <jats:italic toggle=\"yes\">in vivo<\/jats:italic>\n                    . Restoration of LSEC differentiation\n                    <jats:italic toggle=\"yes\">in vivo<\/jats:italic>\n                    promotes HSC quiescence, enhances regression of fibrosis, and prevents progression of cirrhosis. 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