Role of Oxidized LDL and Antioxidants in Atherosclerosis
Atherosclerosis is responsible for more morbidity and mortality than any other single degenerative disease, including cancer. Its clinical expression in the form of myocardial infarction, stroke and peripheral vascular disease accounts for about 50% of all deaths in developed countries. It is a disease of aging, in the sense that the occurrence of clinically significant lesions increases sharply past the 5th decade, but it is equally clear that clinical expression is strongly linked to a number of environmental factors (e.g., hypercholesterolemia, hypertension, cigarette smoking, etc.). Correction of these “risk factors”, especially hypercholesterolemia, has clearly been shown to reduce the number of clinical events. An important point that is often overlooked is that spontaneous atherosclerosis in animals, including non-human primates, is very rare. This stands in contrast to the very significant incidence of cancers in animals and their rising incidence with age. Animals rarely exhibit LDL cholesterol levels over 80 mg/dl; some have levels as low as 5–25 mg/dl. Furthermore, the apparent immunity of animals to atherosclerosis is almost certainly not due to an intrinsic resistance of their vessel wall to the atherogenic process — lesions have been induced in virtually every mammalian species by simply raising the total plasma cholesterol level to a sufficiently high value. Thus there is good reason to indict hypercholesterolemia as a centrally important factor in human atherosclerosis.
KeywordsFoam Cell Oxidative Modification Foam Cell Formation Fatty Streak Smooth Muscle Cell Growth
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