Molecular mechanisms associated with vascular mechanotransduction.
Cardiovascular diseases are the most prevalent cause of death in developed countries. These diseases, including heart attacks and strokes, often result from atherosclerosis, a fatty deposit of cholesterol, blood cells and fibers in the wall of arteries. It has long been known that high blood flow is greatly protective in the vasculature. Arteries exposed to high flow are typically devoid of atherosclerotic lesions. On the contrary, vessel segments exposed to low or oscillatory blood flow are prone to atherosclerotic plaque formation. Using a variety of in vivo, ex vivo, and in vitro techniques, my laboratory investigates how flow confers its atheroprotective effects. We have developed a unique mouse model wherein changes in the local flow environment lead to atherosclerosis regression. Our objective is to understand the molecular mechanisms that underlie this protective effect. Key elements include endothelial cells that sense blood flow and immune cells that contribute to and may reverse plaque growth. Extracellular matrix components may also influence cell motility and function within atherosclerotic lesions. We hope to provide potential insight into new therapeutic options for patients with atherosclerosis.
Keywords: Atherosclerosis, immunology, Cell-cell and cell-matrix interactions