Cardiovascular disease in CVD is the leading cause of mortality in the developed world and contributes to 1/3rd of all-cause mortality in the United States. Cardiac fibrosis is a key pathological feature of most cardiovascular diseases. Excessive deposition of extracellular matrix proteins results in adverse cardiac remodeling, loss of compliance and cardiac function, leading to heart failure. Macrophages are the primary immune cells in the heart and play a wide variety of roles in cardiac physiology and CVD. In response to environmental stimuli, macrophages can mediate pathological inflammatory processes or reparative tissue remodeling, causing alterations in collagen turnover, cardiomyocyte stiffness and altered cardiac metabolism. My work focuses on macrophage fibroblast paracrine signaling events that mediate cardiac fibrosis in cardiovascular disease. We are also interested in taking a systems approach to understand inter organ crosstalk and inflammatory signaling in the pathology of heart failure with preserved ejection fraction (HFpEF).
- BTech/MTech, SASTRA University, India, 2011
- PhD, Johns Hopkins University, School of Medicine, 2016
- Postdoctoral Fellow, Department of Stem Cell and Regenerative Biology, Harvard University, 2019
- Postdoctoral Scholar, University of Pittsburgh, School of Medicine, Vascular Medicine Institute, 2024
Education & Training
- American Heart Association Predoctoral Fellowship (Maggie Wimsatt Memorial Award)
- NHLBI F32
- American Heart Association Career Development Award (declined to accept K99)
- NHLBI K99/R00 Investigating the Role of Macrophages in Heart Failure with Preserved Ejection Fraction, 2024