Pathogenesis of atherosclerosis

Abstract

Two recent developments provide strong support for the role of plasma lipoproteins in plaque formation: plaque stabilization due to rapid removal of cholesterol from macrophage-foam cells has been suggested to explain the rapid cessation of clinical coronary artery disease events after aggressive lipoprotein-modifying therapy; and transgenic mice studies using overexpression and gene knockout of apolipoproteins A-I and E suggest that remnant lipoprotein particles are atherogenic and that apolipoprotein A-I (high-density lipoprotein) can clearly inhibit atherosclerosis development. Two of the more exciting areas of vascular-wall biology at this time are the possibility that endothelial dysfunction may be assessed by measurement of circulating factors (such as atherosclerosis-associated endothelial leukocyte adhesion molecule), and studies of the role of fibrin-like peptides in atherogenesis and coronary artery disease risk assessment.