Advances in role of lipophagy in nonalcoholic fatty liver disease and mechanism of exercise regulation
10.3969/j.issn.1000-4718.2025.01.019
- VernacularTitle:脂噬在非酒精性脂肪性肝病中的作用及运动调节机制的研究进展
- Author:
Senlin LEI
1
;
Xianhui LI
;
Fangjia WU
Author Information
1. 吉首大学体育科学学院,湖南 吉首 416000
- Publication Type:Journal Article
- Keywords:
lipophagy;
nonalcoholic fatty liver disease;
exercise
- From:
Chinese Journal of Pathophysiology
2025;41(1):165-172
- CountryChina
- Language:Chinese
-
Abstract:
Nonalcoholic fatty liver disease(NAFLD)is characterized by the pathological accumulation of lipid droplets(LDs)in the liver and is recognized as a chronic metabolic disorder linked to lifestyle-induced dyslipidemia.Li-pophagy,a specialized form of selective autophagy,targets intracellular LDs for degradation through the autophagy-lyso-some pathway,serving as a critical regulatory mechanism for maintaining hepatic lipid homeostasis.In the context of NAFLD,lipophagy is often impaired,which can affect disease progression.Exercise-regulated lipophagy pathways and factors play a crucial role in alleviating the phenotypes associated with NAFLD,indicating that enhancing lipophagy may be a key target for exercise interventions aimed at improving this condition.This article examines the process of liver-relat-ed lipophagy,focusing on its role in the development of NAFLD.It further elucidates the regulatory effects and mecha-nisms by which exercise influences lipophagy within the pathological context of NAFLD,thereby providing a novel theoreti-cal framework and perspective for clinical intervention and exercise rehabilitation strategies in NAFLD management.The review highlights that the role of lipophagy varies across different stages of NAFLD,with both acute and chronic exercise impacting lipophagy through several mechanisms:modulation of the expression of factors related to LD metabolism,en-hancement of lysosomal function during lipophagy,induction of muscle factor FGF21 secretion to activate lipophagy-relat-ed signaling pathways,and regulation of autophagy-associated epigenetic modifications.
