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 a result of various pathological scenarios such as myocardial infarction, hypertension, obesity, diabetes, aging, and post-traumatic stress disorder.
Heart failure (impaired ventricular pump function) is an eventual outcome of diverse cardiovascular disorders and the leading cause of combined morbidity and mortality in the United States and other developed industrial nations.
The overall approach consists of the generation and analysis of clinically relevant genetic mouse models including a tool mouse enabling tracking of endogenous cardiac exosomes, and conducting 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.