Scavenger receptors in atherosclerosis

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Abstract
—Atherosclerotic vascular disease arises as a consequence,of the deposition and retention of serum lipoproteins in the artery wall. Macrophages in lesions have been shown,to express,6 structurally different scavenger receptors for uptake of modified forms of low-density lipoproteins (LDLs) that promote,the cellular accumulation,of cholesterol. Because cholesterol-laden macrophage foam cells are the primary component of the fatty streak, the earliest atherosclerotic lesion, lipid uptake by these pathways has long been considered a requisite and initiating event in the pathogenesis of atherosclerosis. Although the removal,of proinflammatory,modified LDLs from the artery wall via scavenger receptors would seem beneficial, the pathways distal to scavenger receptor uptake that metabolize the modified lipoproteins appear to become overwhelmed, leading to the accumulation of cholesterol-laden macrophages and establishment of a chronic inflammatory,setting. These observations have led to the current dogma,concerning

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