Research

Coding variants in the extracellular matrix protein SVEP1 (Sushi, Von Willebrand Factor Type A, EGF And Pentraxin Domain Containing 1) have been associated with risk of coronary artery disease and platelet phenotypes in population studies, but the mechanism by which these variants modulates disease risk remain poorly understood. Previous work from the Stitizel lab has identified orphan receptor PEAR1 (Platelet Endothelial Aggregation Receptor 1) as a potential receptor for SVEP1 and has demonstrated that PEAR1 activation may result Akt-mediated proliferation in various cell types. My project will use translational approaches to further characterize the role of the SVEP1-PEAR1 axis in coronary artery disease.

Graduate Publications:

Last Updated: 9/29/2022 11:40:41 AM