My primary research interest is to define the role of lysosomes in cellular homeostasis and response to stress. We are actively interrogating lysosome biology in multiple cell types and disease states including heart failure, atherosclerosis, Alzheimer’s pathogenesis, and diabetes. My lab has uncovered evidence for dysregulation of the lysosome machinery as a major contributor to cardiac myocyte loss in myocardial ischemia-reperfusion injury. Our work has also extended these findings to uncover evidence for lysosome dysfunction in various CNS cell types in Alzheimer’s disease and in pancreatic beta cells in obesity-induced diabetes, underscoring the importance of acquired lysosome dysfunction in triggering multiple chronic diseases that are predisposed by common risk factors. As the PI or co-investigator on studies funded through National funding mechanisms, we have developed the expertise and tools to experimentally perturb and evaluate lysosome biology, concomitantly with disease modeling in in vitro and in vivo systems. Our overarching goal is to develop therapies to harness lysosome function in treating heart failure, cardiometabolic conditions and Alzheimer's disease.

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Heart failure

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