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Atherosclerosis is an inflammatory disease in which the initial cellular event appears to be the localized, but non-propagative, accumulation of cholesterol in the arterial wall. Cell culture studies have demonstrated that oxidized cholesterol derivatives have diverse, but often toxic, biological actions. This oxidized cholesterol has the potential to promote atherosclerosis, but the available clinical evidence suggests that it may be a marker rather than a cause of the disease. To provide a mechanistic understanding of this paradox, we propose that atherosclerosis is initiated by a localized excessive influx of oxidized cholesterol, leading to a progressive accumulation of lipid in the arterial wall. Oxidation of cholesterol by enzymatic or non-enzymatic mechanisms leads to the accumulation of oxysterols which may have biological activities that promote atherosclerosis. In this model, there are two parallel pathways of atherogenesis, a lipid-dependent pathway that leads to the progressive accumulation of cholesterol, and an oxysterol-dependent pathway. The balance between the two pathways may determine the outcome of arterial cholesterol accumulation, and this may explain the apparent opposing effects of cholesterol lowering and oxysterol elevation in the treatment of atherosclerosis.General information
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