Kecheng Zhai^1,2, Yangmengna Gao^1,2, Yu Xiang^1,2, Jiameng Liu^1,2, Shangping Fang^1,2

¹School of Anesthesiology, ²Anesthesia Laboratory and Training Center, Wannan Medical College, Wuhu 241002,  Anhui Province, China.

Address correspondence to: Shangping Fang, Anesthesia Laboratory and Training Center, Wannan  Medical Collegem, No. 22, Wenchang West Road, Higher Education Park, Wuhu 241002, Anhui Province, China. E-mail: 20180041@wnmc.edu.cn.

Acknowledgement: This work was supported by the National College Student Innovation and Entrepreneurship Project (202310368016) and Anhui Province College Student Innovation and Entrepreneurship Project  (S202310368027).

Received October 24, 2024; Accepted January 8, 2025; Published March 31, 2025

Highlights

● Mitochondrial autophagy is essential for maintaining mitochondrial health by selectively degrading damaged mitochondria. This process involves two main pathways: ubiquitin-dependent and ubiquitin-independent autophagy. 

● Sepsis causes organ dysfunction due to infection, with acute lung injury (ALI) being a common secondary condition. ALI is characterized by excessive inflammation in the lungs, leading to mitochondrial dysfunction. 

● Understanding the mechanisms of mitochondrial autophagy can provide new insights for treating sepsis-associated ALI. Continued research could identify novel therapeutic targets to improve outcomes for patients with ALI and sepsis. 

● In the early stages of sepsis-related ALI, mitochondrial autophagy is enhanced. In severe or prolonged cases, excessive mitochondrial autophagy may occur. In the later stages, particularly in severe or chronic cases, mitochondrial autophagy may be impaired or completely lost. 

● Mitochondrial autophagy holds therapeutic potential for the perioperative assessment and management of sepsis-related ALI. Further investigation into this potential is warranted.