摘要
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。
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 macrophage scavenger receptors and TLRs interact may be key to treating atherosclerosis.The article reviewed the role of classical scavenger receptors and TLR4 in ox-LDL uptake and inflammation resporse,in order to provide ideas for finding new targets for treating atherosclerosis.
作者
段兴鹏
刘景丽
王澈
尚德静
DUAN Xingpeng;LIU Jingli;WANG Che;SHANG Dejing(School of Life Science,Liaoning Normal University,Liaoning Dalian 116081,China;School of Chemistry and Chemical Engineering,Liaoning Normal University,Liaoning Dalian 116029,China)
出处
《生物技术进展》
2024年第4期668-675,共8页
Current Biotechnology
基金
国家自然科学基金项目(32070440,32170499)
辽宁省教育厅高等学校基础科研项目(LJKMZ20221406)
辽宁师范大学博士启动项目(2022BSL004)。