内质网应激和自噬在PM_(2.5)诱导的呼吸系统疾病中的作用

Roles of Endoplasmic reticulum stress and autophagy in PM_(2.5) induced respiratory disease

内质网应激和细胞自噬均是细胞维持稳态的重要调节机制。内质网是真核细胞中合成、折叠和运输蛋白质的重要细胞器。当内质网中的蛋白质折叠发生紊乱时,大量未折叠或错误折叠的蛋白质出现积累,引起的后续反应称为内质网应激。当内质网应激无法清除折叠紊乱的蛋白质时,细胞自噬将被激活,以清除这类蛋白质,维持细胞稳态。PM_(2.5)作为一类环境污染物,可激活内质网应激与自噬,引起慢性阻塞性肺疾病、缺血性心脏病、脑血管病等多种疾病。本文就PM_(2.5)激活内质网应激和自噬在呼吸系统疾病中的作用作一综述,旨在为相关疾病的临床治疗提供新思路。

Endoplasmic reticulum stress(ERS)and autophagy are important regulatory mechanisms for cell homeostasis.The endoplasmic reticulum is an important organelle for the synthesis,folding and transport of proteins in eukaryotic cells.When the folding of proteins in the endoplasmic reticulum is disordered,a large number of unfolded or misfolded proteins accumulate,and the subsequent reaction is called ERS.When ERS can't remove the broken proteins,autophagy will be activated to clear these proteins and maintain cell homeostasis.As a class of environmental pollutants,PM_(2.5)can activate ERS and autophagy,causing chronic obstructive pulmonary disease,ischemic heart disease,cerebrovascular disease and other diseases.This article reviews the roles of ERS and autophagy in PM_(2.5)induced respiratory diseases,in order to provide new thoughts for the treatment of respiratory diseases.