Heart failure (impaired ventricular pump function) is an eventual outcome for diverse cardiovascular disorders and the leading cause of combined morbidity and mortality in the United States and other developed industrial nations. The focus of my lab is to understand the molecular and cellular mechanisms that initiate and mediate the pathogenesis of maladaptive cardiac remodeling, such as cardiac hypertrophy and fibrosis as result of various pathological scenarios such as myocardial infarction, hypertension, obesity, diabetes, aging and post-traumatic stress disorder. The overall approach consists of generation and analysis of clinically-relevant genetic mouse models including a tool mouse enabling tracking endogenous cardiac exosomes, and conduct mechanistic studies using cutting-edge technology. The ultimate goal of our efforts is to provide clinical translation for the prevention and treatment of pathological cardiac remodeling from our mechanistic studies.

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