Document Detail


Hepatic endothelial dysfunction and abnormal angiogenesis: new targets in the treatment of portal hypertension.
MedLine Citation:
PMID:  20561700     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Portal hypertension is the main cause of complications in patients with chronic liver disease. Over the past 25 years, progress in the understanding of the pathophysiology of portal hypertension was followed by the introduction of an effective pharmacological therapy, consisting mainly of treatments aimed at correcting the increased splanchnic blood flow. It is only recently that this paradigm has been changed. Progress in our knowledge of the mechanisms of increased resistance to portal blood flow, of the formation of portal-systemic collaterals, and of mechanisms other than vasodilatation maintaining the increased splanchnic blood flow have opened entirely new perspectives for developing more effective treatment strategies. This is the aim of the current review, which focuses on: (a) the modulation of hepatic vascular resistance by correcting the increased hepatic vascular tone due to hepatic endothelial dysfunction, and (b) correcting the abnormal angiogenesis associated with portal hypertension, which contributes to liver inflammation and fibrogenesis, to the hyperkinetic splanchnic circulation, and to the formation of portal-systemic collaterals and varices.
Authors:
Jaume Bosch; Juan G Abraldes; Mercedes Fernández; Juan Carlos García-Pagán
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review     Date:  2010-06-01
Journal Detail:
Title:  Journal of hepatology     Volume:  53     ISSN:  0168-8278     ISO Abbreviation:  J. Hepatol.     Publication Date:  2010 Sep 
Date Detail:
Created Date:  2010-08-17     Completed Date:  2010-12-07     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8503886     Medline TA:  J Hepatol     Country:  England    
Other Details:
Languages:  eng     Pagination:  558-67     Citation Subset:  IM    
Copyright Information:
Copyright 2010 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.
Affiliation:
Hepatic Hemodynamic Laboratory, Liver Unit, Hospital Clínic-IDIBAPS and Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas, Spain. jbosch@clinic.ub.es
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MeSH Terms
Descriptor/Qualifier:
Antioxidants / therapeutic use
Biopterin / analogs & derivatives,  therapeutic use
Endothelium, Vascular / physiopathology
Humans
Hydroxymethylglutaryl-CoA Reductase Inhibitors / therapeutic use
Hypertension, Portal / pathology,  physiopathology,  therapy*
Liver / blood supply,  physiopathology
Neovascularization, Pathologic
Nitric Oxide / metabolism
Prostaglandin-Endoperoxide Synthases / metabolism
Prostaglandins / metabolism
Signal Transduction
Splanchnic Circulation / physiology
Vascular Resistance
Chemical
Reg. No./Substance:
0/Antioxidants; 0/Hydroxymethylglutaryl-CoA Reductase Inhibitors; 0/Prostaglandins; 10102-43-9/Nitric Oxide; 17528-72-2/5,6,7,8-tetrahydrobiopterin; 22150-76-1/Biopterin; EC 1.14.99.1/Prostaglandin-Endoperoxide Synthases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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