My research experience lies at the intersection of cardiovascular inflammation and computational tools for biomedical science.

Moving forward, I am interested in investigating the overlap of cardiovascular disease and immunology. My ultimate goal is to be able to lead a team capable of both (a) identifying in silico and (b) verifying in vitro and in vivo novel pathophysiologies and therapeutic targets in cardiovascular inflammation. My recent work has focused on clonal hematopoiesis of indeterminate potential (CHIP), and I am excited and hopeful that CHIP will provide a new avenue to understand how inflammation at large interacts with cardiovascular disease across the population.

I am currently focused on using whole-genome approaches in mice and humans to understand myeloid cell contributions to cardiovascular disease. For example, our recent publication helps understand how the underlying genetic architecture can impact clonal hematopoiesis.

I have used computational tools in large datasets to explore relationships between clonal hematopoiesis and cardiovascular disease, leading to publications in JCI (aortic valve stenosis) and Circulation: Genomic and Precision Medicine (coronary artery disease anatomy). I have previously used electronic medical record data to identify a connection between celecoxib and aortic valve disease, and I separately performed an unbiased analysis of echocardiographic data on aortic valve disease in a major medical center to identify inequities and diagnostic patterns.

My PhD thesis work used genetic mouse models, bone marrow transplants, and in vitro models to understand the role of immune cells in calcific aortic valve disease (CAVD). We described that a common genetic mutation associated with CAVD leads to increased recruitment of pro-inflammatory monocytes and macrophages, and that these cells then promote a pro-calcific transcriptional program in aortic valve cells.  I continue to be interested in how circulating cell types impact calcification of the aortic valve and lead to aortic valve stenosis.