Our overall hypothesis is that detrimental reprogramming of smooth muscle cells (SMC) destabilizes atherosclerotic plaques and that there are critical genetic determinants of coronary artery disease risk that act in part by impacting SMC phenotypic transitions.
Our ultimate goals are to:
The course from a healthy vessel to myocardial infarction may pass through different pathological features.
PlaqOmics will focus on the role of SMC, specifically in unstable lesions, i.e. erosions, thin-capped fibroatheroma or ruptured plaques (modified from Virmani et al. 2016).