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Hepatology. 2015 May;61(5):1740-6. doi: 10.1002/hep.27376. Epub 2015 Mar 23.

Liver sinusoidal endothelial cells in hepatic fibrosis.

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Division of Gastrointestinal and Liver Disease and the USC Research Center for Liver Diseases, Keck Medicine of the University of Southern California, Los Angeles, CA.

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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)-stimulated, nitric oxide (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.

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