Thesis Advisor
Entering Year
Research: Cardiovascular disease, a leading cause of death in the United States, is primarily driven by atherosclerotic plaque formation. Atherosclerosis progression is
mediated by the deposition of LDL cholesterol in plaque-associated macrophages,
aka foamy or foam cells. Work from the Williams lab has shown that expression of
Trem2, a transmembrane lipid sensor, is enriched in foamy macrophages, and
conditional deletion of Trem2 in these cells significantly reduces plaque burden.
My work involves investigating the mechanisms by which Trem2 expression
mediates foamy macrophage survival and function in atherosclerotic plaque.
