Abstract
Macrophage death in advanced atherosclerotic lesions gives rise to lesional necrosis and plaque instability. Late lesional macrophages accumulate large amounts of unesterified, or “free” cholesterol (FC), and FC loading of macrophages is cytotoxic. Therefore, FC-induced macrophage death in advanced atherosclerosis may represent an important turning point in lesion progression. This brief review summarizes recent findings on the cellular and molecular mechanisms of FC-induced macrophage death. These mechanisms suggest novel therapeutic strategies directed at maintaining plaque stability and inhibiting acute vascular events.
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