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Article
RhoA/Rho-kinase signaling: A therapeutic target in pulmonary hypertension
Vascular Health and Risk Management
  • Scott A. Barman, Philadelphia College of Osteopathic Medicine
  • Shu Zhu, Philadelphia College of Osteopathic Medicine
  • Richard E. White, Philadelphia College of Osteopathic Medicine
Document Type
Article
Publication Date
1-1-2009
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. © 2009 Barman et al, publisher and licensee Dove Medical Press Ltd.
Comments

This article was published in Vascular Health and Risk Management, Volume 5, Pages 663-671.

The published version is available at http://dx.doi.org/10.2147/VHRM.S4711.

Copyright © 2009 the authors and distributed CC-BY.

Citation Information
Scott A. Barman, Shu Zhu and Richard E. White. "RhoA/Rho-kinase signaling: A therapeutic target in pulmonary hypertension" Vascular Health and Risk Management Vol. 5 (2009) p. 663 - 671
Available at: http://works.bepress.com/richard_white/48/