Document Detail

Animal models of pulmonary hypertension: Rho Kinase inhibition.
MedLine Citation:
PMID:  22713173     Owner:  NLM     Status:  Publisher    
Pulmonary Hypertension is a terminology encompassing a range of etiologically different pulmonary vascular diseases. The most common is that termed pulmonary arterial hypertension or PAH; a rare but often fatal disease characterized by a mean pulmonary arterial pressure of >25mmHg. PAH is associated with a complex etiology highlighted by core characteristics of increased pulmonary vascular resistance and elevation of mean pulmonary artery pressure. When sustained, pulmonary vascular remodeling occurs and eventually patients pass away due to right heart failure. Hypoxic pulmonary vasoconstriction is an early event occurring in pulmonary hypertension due to chronic exposure to hypoxia. While the underlying mechanisms of hypoxic pulmonary vasoconstriction may be controversial, a role for Rho A/Rho kinase mediated regulation of intracellular Ca(2+) has been recently identified. Further study suggests that Rho A may have an integral role in other pathophysiological processes such as cell proliferation and migration occurring in all forms of PH. Indeed Rho proteins are known to play essential roles in actin cytoskeleton organization in all eukaryotic cells and thus Rho and Rho-GTPases are implicated in fundamental cellular processes such as cellular proliferation, migration, adhesion, apoptosis and gene expression. This review focuses on providing an overview of the role of RhoA/Rho kinase in currently available animal models of pulmonary hypertension.
Amy L Firth; Il-Whan Choi; Won Sun Park
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2012-6-16
Journal Detail:
Title:  Progress in biophysics and molecular biology     Volume:  -     ISSN:  1873-1732     ISO Abbreviation:  -     Publication Date:  2012 Jun 
Date Detail:
Created Date:  2012-6-20     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0401233     Medline TA:  Prog Biophys Mol Biol     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2012. Published by Elsevier Ltd.
Laboratory of Genetics, Salk Institute for Biological Studies, La Jolla, California, USA.
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