Malondialdehyde (MDA)-modified and oxidized low density lipoproteins (LDL) have been demonstrated in atherosclerotic lesions. Elevated titers of autoimmune antibodies specific for MDA-modified LDL predicted the progression of carotid atherosclerosis and of myocardial infarction. Recently, elevated levels of MDA-modified LDL were detected in the plasma of patients with
ischemic heart disease, whereas, elevated levels of oxidized LDL were detected in the plasma of patients with ischemic heart disease and of heart transplant patients with post-transplant cardiovascular disease. Although increased levels of autoimmune antibodies against oxidatively modified LDL and increased levels of oxidized LDL antigen appear to be associated with atherosclerotic cardiovascular disease, there is to date no direct proof of the causal role of oxidized LDL in atherothrombosis.
However, the decreased risk of cardiovascular disease associated with the administration of antioxidants (e.g. vitamin E), estrogen supplementation and increased levels of high density lipoproteins (HDL) may, at least partially, be due to the inhibition of oxidation of LDL or to the reversal of the atherothrombotic effects of oxidized LDL. To read this article in full you will need to make a payment The role of the monocyte in atherogenesis. I. Transition of blood-borne monocytes into foam cells in fatty lesions. Arterial foam cells with distinctive immunomorphologic and histochemical features of macrophages. Lipoprotein metabolism in the macrophage: implications for cholesterol deposition in atherosclerosis. The pathogenesis of atherosclerosis: an update. The pathogenesis of
atherosclerosis: an update: a perspective for the 1990’s. Risk of thrombosis in human atherosclerotic plaques: role of extracellular lipid, macrophage and smooth muscle cell content. Coronary atherosclerotic wall thickening and vascular reactivity in humans. Elevated high-density lipoprotein levels ameliorate abnormal vasoconstriction in early atherosclerosis. Malondialdehyde-altered protein occurs in atheroma of Watanabe heritable hyperlipidemic rabbits. Evidence for the presence of oxidatively modified low density lipoprotein in
atherosclerotic lesions of rabbit and man. Stimulation with a monoclonal antibody (mAb-4E4) of scavenger receptor-mediated uptake of chemically modified low density lipoproteins by THP-1-derived macrophages enhances foam cell
generation.
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Role of endothelium in thrombosis and hemostasis. Annu Rev Med. 1996; 47: 315-331Article InfoIdentificationDOI: https://doi.org/10.1016/S0021-9150(97)00305-5 Copyright© 1998 Elsevier Science Ireland Ltd. Published by Elsevier Inc. All rights reserved. ScienceDirectAccess this article on ScienceDirectRelated ArticlesHow does oxidized LDL cause atherosclerosis?LDL is thought to be oxidized within the extracellular space of atherosclerotic lesions and then to be bound by scavenger receptors and taken up by macrophages, which become cholesterol-laden foam cells, a major feature of atherosclerotic lesions.
What is a consequence of the oxidation of low density lipoproteins LDLs?Oxidized LDL (oxLDL) represents a variety of modification of both lipid and apolipoprotein B (apoB) components by lipid peroxidation. This promotes atherosclerosis through inflammatory and immunologic mechanisms that lead to the formation of macrophage foam cells.
What happens when LDLs are oxidized?Oxidized LDL triggers inflammation leading to the formation of plaque in the arteries, also known as atherosclerosis. Oxidized LDL may also play a role in increasing the amount of triglycerides the body produces, as well as increasing the amount of fat deposited by the body.
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What is the effect of oxidized low-density lipoproteins (LDLs in atherosclerosis)
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