Association of RhoGDIα with Rac1 GTPase mediates free radical production during myocardial hypertrophy
Open Access
- 15 July 2006
- journal article
- Published by Oxford University Press (OUP) in Cardiovascular Research
- Vol. 71 (2) , 342-351
- https://doi.org/10.1016/j.cardiores.2006.04.005
Abstract
Objective Reactive oxygen species (ROS) contribute to the pathogenesis of myocardial hypertrophy. NADPH oxidase is a major source of ROS production. The small GTPase Rac1 mediates the activation of NADPH oxidase; however, the mechanism of Rac1 activation is incompletely understood. Methods and results Transaortic constriction (TAC, C57/Bl6 mice, 360 μm, 21 days) increased the ratio of heart to body weight from [‰] SHAM 4.16±0.09 to TAC 7.1±0.37, ppConclusions Myocardial hypertrophy is characterized by activation of Rac1 and NADPH oxidase. The association of the regulatory protein RhoGDIα with Rac1 represents a necessary step in the Rac1-dependent release of ROS. Rac1–RhoGDIα binding may represent a target for anti-hypertrophic pharmacologic interventions, potentially by statin treatment.Keywords
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