巨噬细胞吞噬氧化型低密度脂蛋白(oxidized low density lipoprotein,ox-LDL)后形成的泡沫细胞是动脉粥样硬化过程的标志.在巨噬细胞摄取ox-LDL过程中,清道夫受体人类白细胞分化抗原36(cluster of differentiation 36,CD36)、清道夫受体A1(scavenger receptor class A1,SR-A1)、氧化低密度脂蛋白受体 1(lectin like oxidized low density lipoprotein receptor,LOX-1)发挥着重要功能.有研究表明,与炎症相关的巨噬细胞Toll样受体(Toll-like receptors,TLR),如TLR4,通过激发炎症反应影响ox-LDL的摄取,然而两者的调控机制尚不清楚.巨噬细胞清道夫受体和TLR如何相互影响可能是治疗动脉粥样硬化的关键.通过对经典清道夫受体和TLR4在ox-LDL摄取与炎症反应中的作用研究进展进行综述,以期为寻找治疗动脉粥样硬化新的靶点提供思路.
Effects of Macrophage Scavenger Receptors and Toll-like Receptors on Ox-LDL Uptake and Inflammation
Foam cells formed by macrophages after phagocytosis oxidized low density lipoprotein(ox-LDL)are a hallmark of the atherosclerosis.Cluster of differentiation 36(CD36),scavenger receptor class A1(scavenger receptor class A1),SR-A1 and lectin like oxidized low density lipoprotein receptor(LOX-1)played important roles in the uptake of ox-LDL by macrophages.Studies have shown that Toll-like receptors(TLRs)of macrophages associated with inflammation,such as TLR4,could affect ox-LDL uptake by stimulating inflammatory response.However the mechanism of their regulation remains unclear.How macro-phage scavenger receptors and TLRs interact may be key to treating atherosclerosis.The article reviewed the role of classical scav-enger receptors and TLR4 in ox-LDL uptake and inflammation resporse,in order to provide ideas for finding new targets for treat-ing atherosclerosis.
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