My main interest is translational cardiovascular research. My work focus is on myocardial remodeling during heart failure progression when the heart is subjected to chronic pressure overload either in the presence or absence of diabetes mellitus. My goal has been to distinguish between the pathophysiological mechanisms underlying these two comorbidities that frequently co-exist. I have investigated changes in myocardial gene expression, myofilamentary function, ECM changes, and in vivo hemodynamic function, providing an integrative analysis of the cardiac changes. These studies were performed on animal models as in-patients; therefore, I consider myself a researcher with strong interaction between fundamental and clinical research. Recently, my interests have expanded toward unraveling the mechanisms underlying incomplete reverse remodeling, including regression of myocardial hypertrophy in humans after aortic valve replacement and in animal models of reversible banding.