Purpose of review: Scavenger receptor class B type 1 (SR-B1) promotes atheroprotection through its role in HDL metabolism and reverse cholesterol transport in the liver. However, evidence indicates that SR-B1 may impact atherosclerosis through nonhepatic mechanisms.
Recent findings: Recent studies have brought to light various mechanisms by which SR-B1 affects lesional macrophage function and protects against atherosclerosis. Efferocytosis is efficient in early atherosclerotic lesions. At this stage, and beyond its role in cholesterol efflux, SR-B1 promotes free cholesterol-induced apoptosis of macrophages through its control of apoptosis inhibitor of macrophage (AIM). At more advanced stages, macrophage SR-B1 binds and mediates the removal of apoptotic cells. SR-B1 also participates in the induction of autophagy which limits necrotic core formation and increases plaque stability.
Summary: These studies shed new light on the atheroprotective role of SR-B1 by emphasizing its essential contribution in macrophages during atherogenesis as a function of lesion stages. These new findings suggest that macrophage SR-B1 is a therapeutic target in cardiovascular disease.
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