Pathogenesis of atherosclerosis.
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.
Segrest
J P
JP
Department of Medicine, University of Alabama Medical Center, Birmingham.
Anantharamaiah
G M
GM
D001158:Arteries / Q000473:pathology; D001161:Arteriosclerosis / Q000097:blood / Q000473:pathology / Q000503:physiopathology; D003324:Coronary Artery Disease / Q000097:blood / Q000473:pathology / Q000503:physiopathology*; D003331:Coronary Vessels / Q000473:pathology; D004730:Endothelium, Vascular / Q000502:physiology; D006801:Humans; D008074:Lipoproteins / Q000097:blood; D008264:Macrophages / Q000502:physiology; D009131:Muscle, Smooth, Vascular / Q000502:physiology
D008074:Lipoproteins