Lipid peroxidation and atherosclerosis

Lipid peroxidation apparently plays a major role in the pathology of atherosclerosis. Atherosclerosis, which is usually a precondition for CHD, is a degenerative process leading to the accumulation of a variable mixture of substances including lipid in the endothelium of the arteries. This disease is characterized by the formation of a fatty streak and the accumulation of cells loaded with lipid: the foam cells. These cells are believed to arise from white blood cell-derived macrophages or arterial smooth muscle cells. Most of the lipid in the foam cells is in the form of LDL particles. Although research has determined that LDL receptors are responsible for the uptake of LDL by cells, the arterial uptake of LDL, which leads to development of foam cells, occurs by a different pathway. It is only when the LDL particles have undergone oxidative modification that they are available for uptake by macrophages via the scavenger receptor. During the course of oxidative modification, LDL cholesterol acquires various biological properties not present in native LDL that make it a potentially important mediator, promoting atherogenesis. The LDL, once oxidized, becomes cytotoxic and causes local cellular damage to the endothelium. This process, which enhances LDL uptake to generate foam cells, is considered one of the earliest events in atherogenesis (Figure 2).

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