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dc.contributor.authorBarman, Scott A
dc.contributor.authorZhu, Shu
dc.contributor.authorWhite, Richard E.
dc.date.accessioned2010-09-24T22:03:23Z
dc.date.available2010-09-24T22:03:23Z
dc.date.issued2009-08-26en_US
dc.identifier.citationVasc Health Risk Manag. 2009 Aug 20; 5:663-671en_US
dc.identifier.issn1178-2048en_US
dc.identifier.pmid19707285en_US
dc.identifier.urihttp://hdl.handle.net/10675.2/119
dc.description.abstractPulmonary 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.
dc.rightsThe PMC Open Access Subset is a relatively small part of the total collection of articles in PMC. Articles in the PMC Open Access Subset are still protected by copyright, but are made available under a Creative Commons or similar license that generally allows more liberal redistribution and reuse than a traditional copyrighted work. Please refer to the license statement in each article for specific terms of use. The license terms are not identical for all articles in this subset.en_US
dc.subject.meshAnimalsen_US
dc.subject.meshAntihypertensive Agents / adverse effects / therapeutic useen_US
dc.subject.meshBlood Pressure / drug effectsen_US
dc.subject.meshDisease Models, Animalen_US
dc.subject.meshEvidence-Based Medicineen_US
dc.subject.meshHumansen_US
dc.subject.meshHypertension, Pulmonary / drug therapy / enzymology / physiopathologyen_US
dc.subject.meshMuscle, Smooth, Vascular / drug effects / enzymology / physiopathologyen_US
dc.subject.meshProtein Kinase Inhibitors / adverse effects / therapeutic useen_US
dc.subject.meshSignal Transduction / drug effectsen_US
dc.subject.meshTreatment Outcomeen_US
dc.subject.meshVascular Resistance / drug effectsen_US
dc.subject.meshVasoconstriction / drug effectsen_US
dc.subject.meshrho-Associated Kinases / antagonists & inhibitors / metabolismen_US
dc.subject.meshrhoA GTP-Binding Protein / metabolismen_US
dc.titleRhoA/Rho-kinase signaling: a therapeutic target in pulmonary hypertension.en_US
dc.typeJournal Articleen_US
dc.typeResearch Support, N.I.H., Extramuralen_US
dc.typeResearch Support, Non-U.S. Gov'ten_US
dc.typeReviewen_US
dc.identifier.pmcidPMC2731064en_US
dc.contributor.corporatenameDepartment of Pharmacology and Toxicologyen_US
refterms.dateFOA2019-04-09T16:24:19Z
html.description.abstractPulmonary 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.


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