The oxidation hypothesis of atherosclerosis: an update.
Hypercholesterolemia is associated with an increased risk of atherosclerosis. The oxidation hypothesis suggests that oxidative modification of lipoprotein, and in particular low-density lipoprotein (LDL), increases its atherogenicity by altering receptor-mediated uptake by cells in the intima of blood vessels. Oxidized LDL is taken up by scavenger receptors on monocytes, smooth muscle cells, and macrophages in an uncontrolled process leading to accumulation of lipid and the formation of foam cells, an early feature of atherosclerotic plaque. Recent research on the oxidation of LDL lipids, the effect of antioxidants, hypertensives, and other agents, the interaction of LDL with extrinsic factors, as well as patient studies which bear on the oxidation hypothesis, are summarised in this review.
Westhuyzen
J
J
Department of Pathology, Royal Brisbane Hospital, Australia.
D000959:Antihypertensive Agents / Q000494:pharmacology; D000975:Antioxidants / Q000494:pharmacology; D001161:Arteriosclerosis / Q000209:etiology*; D002784:Cholesterol / Q000378:metabolism; D004032:Diet; D005609:Free Radicals / Q000494:pharmacology; D006801:Humans; D008077:Lipoproteins, LDL / Q000494:pharmacology*; D008264:Macrophages / Q000378:metabolism; D008956:Models, Chemical
D000959:Antihypertensive Agents; D000975:Antioxidants; D005609:Free Radicals; D008077:Lipoproteins, LDL; C099252:oxidized low density lipoprotein; D002784:Cholesterol