Sorbonne Universités, INSERM, Institute of Cardiometabolism and Nutrition (ICAN), UMR_S1166, Paris, France.
Curr Opin Lipidol. 2022 Jun 1;33(3):167-174. doi: 10.1097/MOL.0000000000000822. Epub 2022 Mar 7.
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 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.
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.
清道夫受体 B 类 1 型（SR-B1）通过其在 HDL 代谢和肝脏中胆固醇逆向转运中的作用促进动脉粥样硬化保护。然而，有证据表明，SR-B1 可能通过非肝脏机制影响动脉粥样硬化。
最近的研究揭示了 SR-B1 通过影响病变巨噬细胞功能和预防动脉粥样硬化的各种机制。噬作用在早期动脉粥样硬化病变中是有效的。在这个阶段，除了其在胆固醇外排中的作用外，SR-B1 通过其对巨噬细胞凋亡抑制剂（AIM）的控制促进巨噬细胞中游离胆固醇诱导的凋亡。在更晚期，巨噬细胞 SR-B1 结合并介导清除凋亡细胞。SR-B1 还参与自噬的诱导，自噬限制坏死核心形成并增加斑块稳定性。
这些研究通过强调 SR-B1 在动脉粥样硬化发生过程中作为病变阶段的功能在巨噬细胞中的重要作用，为 SR-B1 的动脉粥样硬化保护作用提供了新的认识。这些新发现表明，巨噬细胞 SR-B1 是心血管疾病的治疗靶点。
