内质网是参与蛋白质合成、折叠、脂质代谢和Ca2+ 储存以及运输新肽链的重要细胞器。在应激状态下干扰内质网稳态,可引发内质网应激(endoplasmic reticulum stress,ERS)。而内质网应激通过对未折叠蛋白质反应的激活,达到维持内质网稳态并恢复细胞功能。自噬(autophagy)通常被认为是一种细胞生存机制,在饥饿等应激状态下,自噬可被启动以清除细胞中受损细胞器、蛋白质聚集体或为细胞提供能量。研究显示,内质网应激可以调节自噬,而自噬又可以在不同的情况下诱导细胞的生存,干预疾病的发生发展。因此,本文根据最新研究进展综述内质网应激在细胞自噬调控中的作用及其分子机制。

Endoplasmic reticulum (ER) is a crucial organelle involved in protein synthesis, folding, lipid metabolism, Ca2+ storage and the transport of nascent peptide chains. Disturbing ER homeostasis under stress can lead to endoplasmic reticulum stress (ERS), which maintains ER homeostasis and restores cell function by activating the unfolded protein response. Autophagy is generally considered a cellular survival mechanism, which can be initiated under stress conditions like starvation to remove damaged organelles, protein aggregates or provide energy for the cells. Studies have shown that ERS regulates autophagy, which induces cell survival or intervenes in the development of diseases under different circumstances. Therefore, this article reviews recent progress on the role and molecular mechanisms of ERS in autophagy regulation.