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Our long-standing interest is to elucidate mechanisms by which G-protein signaling regulation plays a role in physiological and pathophysiological adaptations of the cardiovascular and renal systems.
Abnormal G-protein signaling contributes to the development and establishment of diseases of the cardiovascular and renal systems, including hypertension, chronic kidney diseases, heart failure, diabetes, and stroke. Accordingly, receptors that activate G-protein signaling pathways remain predominant therapeutic targets of cardiovascular and renal disease medications, including angiotensin receptor blockers and beta-adrenergic receptor blockers. However, current therapies are inadequate as morbidity and mortality of these diseases continue to rise worldwide.
The specific focus of research in our laboratory is to unravel novel mechanisms whereby regulation and dysregulation of G-protein signaling by regulator of G-protein signaling (RGS) proteins are involved in normal functions and diseases of the cardiovascular and renal systems. To this end, we employ an integrative physiology approach, including the use of small animal disease models, mouse genetics (knock-outs, knock-ins, transgenics, and humanized mice), telemetric blood pressure and heart rate recordings, sympathetic nerve recordings, laser-Doppler flowmetry, ex-vivo studies of the microcirculation, molecular and cellular biology, whole organ and single-cell calcium imaging, and confocal video microscopy.
Our ultimate goal is to gain more insight into the underlying causes of cardiovascular and renal diseases, which may lead to the identification of novel targets for developing new and more effective therapeutics.