[Atherosclerosis--the molecular background]

The clinical manifestations of atherosclerosis, such as stroke and coronary heart disease, are the major cause of death and disability in the western world. Recent technological progress in cell and molecular biology have provided new opportunities of studying the basic biological mechanisms involved in atherogenesis. Several lines of evidence suggest that the macrophage accumulation of cholesterol in atherosclerotic plaques occur as a result of lipid peroxidation. Macrophages lack a receptor for normal low density lipoprotein (LDL), but express a high affinity receptor for oxidized LDL - the scavenger receptor. Oxidized LDL has also been found to be cytotoxic to endothelial cells and to promote the adhesion of monocytes to the endothelium. Growth in plaque size is chiefly due to a proliferation of smooth muscle cells. Studies using a variety of hybridization techniques have demonstrated expression of different growth factor genes in atherosclerotic plaques. It has also been shown that cultured smooth muscle cells have the capacity to produce growth factors, and that this production is subject to factors associated with known risk factors for cardiovascular disease.