巨噬细胞自噬调节急性肺损伤/急性呼吸窘迫综合征的研究进展
Research progress of macrophage autophagy in regulating acute lung injury/acute respiratory distress syndrome
宋雨彤 1王晓芝1
作者信息
- 1. 滨州医学院附属医院重症医学科,山东滨州 256600
- 折叠
摘要
急性肺损伤(ALI)/急性呼吸窘迫综合征(ARDS)是一种发病率和病死率较高的危重临床综合征.巨噬细胞作为先天免疫的重要组成部分,在炎症反应和免疫系统稳态的调节中发挥着关键作用.自噬是在应激条件下启动的自我保护机制.巨噬细胞自噬激活通过多种途径影响ALI/ARDS的过程,包括调节巨噬细胞极化、调节巨噬细胞吞噬、抑制NOD样受体家族结构域3(NLRP3)炎症小体形成、调节内质网应激(ERS)、调节哺乳动物雷帕霉素靶蛋白(mTOR)信号,为减轻ALI/ARDS提供的新的治疗靶点.
Abstract
Acute lung injury(ALI)/acute respiratory distress syndrome(ARDS)is a critical clinical syndrome with high morbidity and mortality.Macrophages,as an important part of innate immunity,play a key role in the regulation of inflammatory reaction and immune system homeostasis.Autophagy is a self-protection mechanism initiated under stress conditions.Macrophage autophagy activation affects ALI/ARDS processes through a variety of pathways,including regulation of macrophage polarization,regulation of macrophage phagocytosis,inhibition of NOD-like receptor family domain 3(NLRP3)inflammasome formation,regulation of endoplasmic reticulum stress(ERS),and regulation of mammalian target of rapamycin(mTOR)signaling.Macrophage autophagy activation provides a new therapeutic target for alleviating ALI/ARDS.
关键词
巨噬细胞/自噬/急性呼吸窘迫综合征/急性肺损伤Key words
Macrophage/Autophagy/Acute respiratory distress syndrome/Acute lung injury引用本文复制引用
基金项目
山东省自然科学基金(ZR2022MH012)
出版年
2024
国家科技期刊平台
NSTL
万方数据