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CD36 在动脉粥样硬化中的作用:病理生理机制与治疗意义。

CD36 in Atherosclerosis: Pathophysiological Mechanisms and Therapeutic Implications.

机构信息

Department of Preventive Medicine, School of Public Health, Zunyi Medical University, Zunyi, Guizhou, China.

Halal Research Center of IRI, FDA, Tehran, Iran.

出版信息

Curr Atheroscler Rep. 2020 Aug 9;22(10):59. doi: 10.1007/s11883-020-00870-8.

DOI:10.1007/s11883-020-00870-8
PMID:32772254
Abstract

PURPOSE OF REVIEW

Atherosclerosis is a chronic disease characterized by lipid retention and inflammation in the artery wall. The retention and oxidation of low-density lipoprotein (LDL) in sub-endothelial space play a critical role in atherosclerotic plaque formation and destabilization. Oxidized LDL (ox-LDL) and other modified LDL particles are avidly taken up by endothelial cells, smooth muscle cells, and macrophages mainly through several scavenger receptors, including CD36 which is a class B scavenger receptor and membrane glycoprotein.

RECENT FINDINGS

Animal studies performed on CD36-deficient mice suggest that deficiency of CD36 prevents the development of atherosclerosis, though with some debate. CD36 serves as a signaling hub protein at the crossroad of inflammation, lipid metabolism, and fatty acid metabolism. In addition, the level of soluble CD36 (unattached to cells) in the circulating blood was elevated in patients with atherosclerosis and other metabolic disorders. We performed a state-of-the-art review on the structure, ligands, functions, and regulation of CD36 in the context of atherosclerosis by focusing on the pathological role of CD36 in the dysfunction of endothelial cells, smooth muscle cells, monocytes/macrophages, and platelets. Finally, we highlight therapeutic possibilities to target CD36 expression/activity in atherosclerosis.

摘要

综述目的

动脉粥样硬化是一种慢性疾病,其特征是动脉壁中的脂质蓄积和炎症反应。低密度脂蛋白(LDL)在血管内皮下的蓄积和氧化在动脉粥样硬化斑块的形成和不稳定中起着关键作用。氧化型 LDL(ox-LDL)和其他修饰的 LDL 颗粒主要通过几种清道夫受体被内皮细胞、平滑肌细胞和巨噬细胞摄取,包括 CD36,它是一种 B 型清道夫受体和膜糖蛋白。

最近的发现

在 CD36 缺陷型小鼠上进行的动物研究表明,CD36 的缺乏可阻止动脉粥样硬化的发生,但存在一些争议。CD36 作为一种信号枢纽蛋白,位于炎症、脂质代谢和脂肪酸代谢的交汇点。此外,在动脉粥样硬化和其他代谢紊乱患者的循环血液中,可溶性 CD36(未附着于细胞)的水平升高。我们通过关注 CD36 在血管内皮细胞、平滑肌细胞、单核细胞/巨噬细胞和血小板功能障碍中的病理作用,就 CD36 在动脉粥样硬化中的结构、配体、功能和调节进行了最新的综述。最后,我们强调了针对 CD36 表达/活性的治疗可能性在动脉粥样硬化中的应用。

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