巨噬细胞程序性死亡在动脉粥样硬化中的研究进展
作者:
作者单位:

1.哈尔滨医科大学, 黑龙江 哈尔滨 150081;2.哈尔滨医科大学附属第一医院, 黑龙江 哈尔滨 150001

作者简介:

通讯作者:

刘文秀,E-mail:hitlqn@126.com;Tel:0451-85555723

中图分类号:

R543.5

基金项目:

国家自然科学基金(No:81700318);大学生创新创业训练计划项目(No:S202110226068,No:202210226120)


Advance on the roles of programmed cell death of macrophages in atherosclerosis
Author:
Affiliation:

1.Harbin Medical University, Harbin, Heilongjiang 150081, China;2.The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, China

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    摘要:

    动脉粥样硬化(AS)是大多数心血管疾病的主要病理基础,是一种由于脂质沉积、泡沫细胞形成等多种因素诱发的慢性无菌性炎症过程。巨噬细胞作为AS病变的主要免疫细胞群,在所有阶段都发挥着关键作用。因此,调控巨噬细胞活动可能成为调节AS进程的有效方法。近年来,随着对细胞程序性死亡的研究逐渐深入,巨噬细胞程序性死亡在AS的发生、转归过程中的重要作用逐渐成为热点。巨噬细胞程序性死亡是由胞内相关基因调控的分子程序所介导的死亡过程,包括凋亡、焦亡、自噬、坏死性凋亡、铁死亡及PARP-1依赖性细胞死亡等。该文对巨噬细胞程序性死亡的基本机制及其各种程序性死亡间的相互作用在AS中的研究进展进行综述,为AS的防治提供新策略。

    Abstract:

    Atherosclerosis (AS), a chronic and aseptic inflammatory process induced by various factors such as lipid deposition and foam cell formation, is the main pathological basis of most cardiovascular diseases. As the major immune cells in AS lesions, macrophages play a key role in all stages of AS. Thus, modulating the activity of macrophages may be an effective way to intervene the progression of AS. In recent years, with the gradual deepening of the research on programmed cell death, the critical roles of programmed cell death of macrophages in the occurrence and outcome of AS have gradually become a hot topic. Programmed cell death of macrophages is a death process mediated by genetically controlled molecular events, and it includes apoptosis, pyroptosis, autophagy, necroptosis, ferroptosis, parthanatos, and among others. In this review, we summarize the fundamental mechanism underlying programmed cell death of macrophages and the advance on the roles of interactions among all forms of programmed cell death in AS, with a view to providing new strategies for the prevention and treatment of AS.

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张皓南,任博文,纪元浩,谷佳鑫,郑子琦,刘文秀.巨噬细胞程序性死亡在动脉粥样硬化中的研究进展[J].中国现代医学杂志,2023,(8):43-49

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  • 收稿日期:2022-07-01
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  • 在线发布日期: 2023-12-04
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