Dominique Thabut a b, Vijay Shah a
Received 21 April 2010; received in revised form 7 July 2010; accepted 12 July 2010. published online 02 August 2010.
Accepted Manuscript
Abstract
Portal hypertension accounts for the majority of morbidity and mortality that is encountered in patients with cirrhosis. Portal hypertension is initiated in large part through increases in intrahepatic vascular resistance. Fibrosis, regenerative nodule formation, and intrahepatic vasoconstriction are classical mechanisms that account for increased intrahepatic vascular resistance in cirrhosis. Recent data suggests that intrahepatic angiogenesis and sinusoidal remodeling could also be involved in sinusoidal resistance, fibrosis, and portal hypertension. While angiogenesis is defined as the formation of new vessels deriving from existing ones, sinusoidal remodeling in its pathological form associated with cirrhosis is characterized by increased mural coverage of vessels by contractile HSC. Most attention on the mechanisms of these processes has focused on the liver sinusoidal endothelial cell (SEC), the hepatic stellate cell (HSC), and the paracrine signaling pathways between these two cell types. Interventions that target these vascular structural changes have beneficial effects on portal hypertension and fibrosis in some animal studies which has stimulated interest for pursuing parallel studies in humans with portal hypertension.
Keywords: Portal hypertension, cirrhosis, angiogenesis, vascular remodeling, receptor tyrosine kinase
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a Gastroenterology Research Unit, Advanced Liver Disease Study Group, Fiterman Center for Digestive Diseases, Mayo Clinic, Rochester, MN, USA.
b Université Pierre et Marie Curie, AP-HP, Service d’Hépato-Gastroentérologie, Groupe Hospitalier Pitié-Salpêtrière, Paris, FRANCE.
PII: S0168-8278(10)00632-X
doi:10.1016/j.jhep.2010.07.004
© 2010 Published by Elsevier Inc.
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