摘要
动脉粥样硬化(AS)是由脂质代谢异常引起的慢性炎症性疾病,是心血管疾病的病理生理基础。细胞凋亡是人体维持内环境稳态的重要调节机制,在AS疾病过程中具有重要作用。内皮细胞(VECs)凋亡可导致血管内皮损伤促进脂质沉积,血管平滑肌细胞(VSMCs)和巨噬细胞凋亡在疾病早期可减少斑块形成,在晚期可引起斑块破裂。诸多因素参与调控细胞凋亡,包括:细胞外囊泡、线粒体、巨噬细胞极化等。本文重点总结上述3类细胞凋亡在AS中的作用及分子机制,以期为AS的治疗提供新思路。
Atherosclerosis(AS)is a chronic inflammatory disease caused by abnormal lipid metabolism,which is the pathophysiological basis of cardiovascular diseases.Apoptosis is an important regulatory mechanism for maintaining homeostasis and plays important roles in AS pathogenesis.In the course of AS,apoptosis of endothelial cells(VECs)leads to vascular endothelial damage and promotes lipid deposition;apoptosis of vascular smooth muscle cells(VSMCs)and macrophages can reduce plaque formation in the early stage and increase plaque rupture and instability in the late stage.There are many factors involved in the regulation of apoptosis,including extracellular vesicles,mitochondria,and macrophage polarization.In this paper,the roles and molecular mechanisms of apoptosis in AS are summarized in order to provide novel ideas for the treatment of AS.
作者
李何玉
王越
汪颖
李靖
曲鹏
LI Heyu;WANG Yue;WANG Ying;LI Jing;QU Peng(Heart and Cardiovascular Research Laboratory,the Second Hospital of Dalian Medical University,Dalian 116023,China)
出处
《大连医科大学学报》
CAS
2023年第6期527-531,537,共6页
Journal of Dalian Medical University
基金
国家自然科学基金项目(81670406,91739119,81900223)
辽宁省博士科研启动基金计划项目(2021-BS-208)
大医二院-中科院大连化物所“个体化诊疗协同创新中心”联合资助基金(202006)
