Abstract
(First of Two Parts*)RECENT research on the pathogenesis of atherosclerosis has focused on the physicochemical nature of the arterial wall and on the roles of smooth-muscle cells, serum lipoproteins and defects in cellular metabolism of cholesterol that lead to early atherosclerosis. Smooth-muscle-cell proliferation is widely believed to be the initial cellular event in the pathogenesis of atherosclerosis.1 A stimulus, such as an injury, a chemical or a virus, is thought to cause smooth-muscle cells to migrate into the intima, where they may transform, proliferate, produce connective tissue and lipid and thus initiate the early lesion. Cellular isoenzyme typing . . .
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