内质网自噬的作用机制
作者: |
1郑婉秋,
1李烁,
1吴金峰,
1陈文佳
1 哈尔滨医科大学附属第一医院心内科,哈尔滨 150001 |
通讯: |
陈文佳
Email: chenwenjia0725@163.com |
DOI: | 10.3978/j.issn.2095-6959.2022.06.030 |
基金: | 国家自然科学基金(81800419);黑龙江省自然科学基金青年科学基金(QC2017104)。 |
摘要
Mechanism of endoplasmic reticulum autophagy
CorrespondingAuthor: CHEN Wenjia Email: chenwenjia0725@163.com
DOI: 10.3978/j.issn.2095-6959.2022.06.030
Foundation: This work was supported by the National Natural Science Foundation (81800419) and Young Science Foundation of Natural Science Foundation of Heilongjiang Province (QC2017104), China.
Abstract
Endoplasmic reticulum autophagy (ER-phagy) refers to the process of regulating the fragmentation of the endoplasmic reticulum and transporting it to lysosomes for degradation, which acts to degrade excess ER membranes and maintain the homeostasis of ER mass and capacity. The receptors mediating ER-phagy include FAM134B, RTN3, SEC62, TEX264, and CCPG1. ER-phagy is significantly enhanced when the body undergoes cell starvation, ER stress, unfolded protein aggregation, and bacterial and viral infections. ER-phagy plays an important role in the processes of cell growth and development, differentiation, inflammation, and immune defense. ER-phagy is involved in the occurrence and development of numerous diseases, such as cardiovascular diseases, tumors, neurological diseases, and infectious diseases. It is of great clinical significance to deeply explore the mechanism of ER-phagy in diseases and to study the effects of intervening ER-phagy on diseases and prognostic outcomes.