An update on the pathogenesis of atherosclerosis (principles of prevention, intervention, retardation, and regression).
The major life-threatening ischemic events in heart and brain are precipitated by the plaque. Thrombosis in the muscular arteries and rupture of the large elastic arteries usually follows fracture or ulceration of the plaque's fibrous cap. The smooth muscle cell (SMC) participates in many aspects of the atherosclerotic process: lipid uptake, synthesis of plaque components, and cell proliferation. The latter is a particularly significant aspect of the disease. High serum cholesterol levels stimulate proliferation of arterial medical cells; lower-density lipoproteins (LDL and B-VLDL) induce ingress and storage of cholesteryl ester in the arterial intima. These effects are inhibited by high-density lipoproteins (HDL). Endothelial injury may be an important part of the pathogenesis of some atherosclerotic plaques because powerful growth factors liberated from circulating monocytes, injured endothelial cells, and platelets, actively stimulate SMC proliferation, even when other risk factors are absent.
Department of Pathology, University of Chicago Medical Center, Illinois.
R W
RW
Wissler
D
D
Vesselinovitch
D000818:Animals; D003324:Coronary Artery Disease / Q000150:complications / Q000473:pathology*; D004195:Disease Models, Animal; D006801:Humans; D008253:Macaca mulatta; D012106:Research