Role of endoplasmic reticulum autophagy in acute lung injury

Shiping Liu; Xiaoyu Fang; Ruiyao Zhu; Jing Zhang; Huijuan Wang; Jiaxi Lei; Chaoqun Wang; Lu Wang; Liying Zhan

doi:10.3389/fimmu.2023.1152336

Role of endoplasmic reticulum autophagy in acute lung injury

Front Immunol. 2023 May 17:14:1152336. doi: 10.3389/fimmu.2023.1152336. eCollection 2023.

Authors

Shiping Liu¹, Xiaoyu Fang¹, Ruiyao Zhu², Jing Zhang¹, Huijuan Wang¹, Jiaxi Lei¹, Chaoqun Wang³, Lu Wang¹, Liying Zhan¹

Affiliations

¹ Department of Critical Care Medicine, Renmin Hospital of Wuhan University, Wuhan, China.
² Department of Infection Prevention and Control, Renmin Hospital of Wuhan University, Wuhan, China.
³ College of Life Sciences, Wuhan University, Wuhan, China.

Abstract

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS), the prime causes of morbidity and mortality in critically ill patients, are usually treated by general supportive treatments. Endoplasmic reticulum autophagy (ER-phagy) maintains cellular homeostasis by degrading damaged endoplasmic reticulum (ER) fragments and misfolded proteins. ER-phagy is crucial for maintaining ER homeostasis and improving the internal environment. ER-phagy has a particular role in some aspects, such as immunity, inflammation, cell death, pathogen infection, and collagen quality. In this review, we summarized the definition, epidemiology, and pathophysiology of ALI/ARDS and described the regulatory mechanisms and functions of ER-phagy as well as discussed the potential role of ER-phagy in ALI/ARDS from the perspectives of immunity, inflammation, apoptosis, pathogen infection, and fibrosis to provide a novel and effective target for improving the prognosis of ALI/ARDS.

Keywords: ALI; ARDS; ER stress; ER-phagy; ER-phagy receptor; immunity; inflammation.

Publication types

Review
Research Support, Non-U.S. Gov't

MeSH terms

Acute Lung Injury* / metabolism
Autophagy / physiology
Endoplasmic Reticulum / metabolism
Endoplasmic Reticulum Stress* / physiology
Humans
Inflammation / metabolism

Grants and funding

This work was supported by grants from the National Key Research and Development Program of China (2021YFC2501800) and National Natural Science Foundation of China (82102245).