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Vasc Health Risk Manag. 2009;5:663-71. Epub 2009 Aug 20.

RhoA/Rho-kinase signaling: a therapeutic target in pulmonary hypertension.

Author information

  • 1Department of Pharmacology and Toxicology, Medical College of Georgia, Augusta, Georgia 30912, USA. sbarman@mcg.edu

Abstract

Pulmonary arterial hypertension (PAH) is a devastating disease characterized by progressive elevation of pulmonary arterial pressure and vascular resistance due to pulmonary vasoconstriction and vessel remodeling as well as inflammation. Rho-kinases (ROCKs) are one of the best-described effectors of the small G-protein RhoA, and ROCKs are involved in a variety of cellular functions including muscle cell contraction, proliferation and vascular inflammation through inhibition of myosin light chain phosphatase and activation of downstream mediators. A plethora of evidence in animal models suggests that heightened RhoA/ROCK signaling is important in the pathogenesis of pulmonary hypertension by causing enhanced constriction and remodeling of the pulmonary vasculature. Both animal and clinical studies suggest that ROCK inhibitors are effective for treatment of severe PAH with minimal risk, which supports the premise that ROCKs are important therapeutic targets in pulmonary hypertension and that ROCK inhibitors are a promising new class of drugs for this devastating disease.

KEYWORDS:

Rho-kinase; fasudil; pulmonary arterial hypertension; vasoconstriction

PMID:
19707285
[PubMed - indexed for MEDLINE]
PMCID:
PMC2731064
Free PMC Article

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