Atherosclerosis, the formation of plaque inside arterial wall, is the leading cause of death and disability in the United States and throughout the world. Atherosclerotic lesions develop in the regions of curvature, bifurcation, and branching of vessels, where fluid shear stress is low. In contrast, steady laminar flow associated with high fluid shear stress within the large straight arteries is atheroprotective.
Our research goal is to elucidate the molecular mechanisms of atherosclerosis and to identify the key molecules and signal pathways in the atheroprotective programs of laminar flow. Our recent studies have demonstrated that histone deacetylase 5 (HDAC5) plays an important role in regulation of laminar flow-sensitive genes. Current projects focus on exploring the mechanisms by which HDAC5 and other chromatin-modifying enzymes control gene transcription in vascular endothelial cells in response to laminar flow. Our studies may provide insights into the pathogenesis of atherosclerosis and lead to the development of new therapies to prevent/treat atherosclerotic disease.