Possible Rotation Projects:
- Role of medium chain fatty acid GPCRs in macrophage polarization and profibrotic signaling.
- Macrophage – fibroblast crosstalk in pathological tissue fibrosis (heart failure with preserved ejection fraction model)
- Myeloid trained immunity in heart failure – role of SCFA metabolites butyrate in macrophage trained immunity and HDAC modulation
Cardiovascular disease in CVD is the leading cause of mortality in the 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. To this end, we study chemosensory GPCRs in macrophages. 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).