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Hepatol Int. 2018 Feb;12(Suppl 1):11-23. doi: 10.1007/s12072-017-9826-x. Epub 2017 Oct 26.

Biology of portal hypertension.

Author information

1
Department of Internal Medicine, Section of Digestive Diseases, Yale University School of Medicine, 1080 LMP, 333 Cedar St., New Haven, CT, 06520, USA.
2
Department of Internal Medicine, Section of Digestive Diseases, Yale University School of Medicine, 1080 LMP, 333 Cedar St., New Haven, CT, 06520, USA. yasuko.iwakiri@yale.edu.

Abstract

Portal hypertension develops as a result of increased intrahepatic vascular resistance often caused by chronic liver disease that leads to structural distortion by fibrosis, microvascular thrombosis, dysfunction of liver sinusoidal endothelial cells (LSECs), and hepatic stellate cell (HSC) activation. While the basic mechanisms of LSEC and HSC dysregulation have been extensively studied, the role of microvascular thrombosis and platelet function in the pathogenesis of portal hypertension remains to be clearly characterized. As a secondary event, portal hypertension results in splanchnic and systemic arterial vasodilation, leading to the development of a hyperdynamic circulatory syndrome and subsequently to clinically devastating complications including gastroesophageal varices and variceal hemorrhage, hepatic encephalopathy from the formation of portosystemic shunts, ascites, and renal failure due to the hepatorenal syndrome. This review article discusses: (1) mechanisms of sinusoidal portal hypertension, focusing on HSC and LSEC biology, pathological angiogenesis, and the role of microvascular thrombosis and platelets, (2) the mesenteric vasculature in portal hypertension, and (3) future directions for vascular biology research in portal hypertension.

KEYWORDS:

Endothelial dysfunction; Hyperdynamic circulation; Platelets; Thrombosis

PMID:
29075990
DOI:
10.1007/s12072-017-9826-x
[Indexed for MEDLINE]

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