Role of innate immune mechanisms triggered by mitochondrial DNA release in metabolic dysfunction-associated fatty liver disease and targeted intervention strategies
- VernacularTitle:线粒体DNA释放触发的先天免疫机制在代谢相关脂肪性肝病中的作用及靶向干预策略
- Author:
Yu ZHOU
1
;
Kaiyang LI
1
;
Mei YANG
2
;
Qi ZHAO
3
;
Yiming ZHAO
1
;
Fei ZHANG
1
;
Qian WANG
1
Author Information
- Publication Type:Review
- Keywords: Metabolic Dysfunction-Associated Fatty Liver Disease; DNA， Mitochondrial; Immunity， Innate; Signal Transduction
- From: Journal of Clinical Hepatology 2026;42(8):1960-1966
- CountryChina
- Language:Chinese
- Abstract: Metabolic dysfunction-associated fatty liver disease （MAFLD） is the most prevalent chronic liver disease worldwide， with a complex pathogenesis. Mitochondria play a pivotal role in this disease process， and studies have confirmed that mitochondrial dysfunction can exacerbate metabolic disorders and induce innate immune imbalance， while mitochondrial DNA （mtDNA） is the core molecule mediating these two pathological effects. After the abnormal release of mtDNA， it can be recognized by intracellular pattern recognition receptors， which in turn triggers innate immune responses and causes tissue damage， forming a pathological pathway of “mtDNA release-immune activation-tissue damage”. Currently， there is a lack of systematic reviews summarizing the mechanism of action of this pathway in different stages of MAFLD and the intervention strategies targeting this pathway. This article systematically reviews the core molecular mechanism of this pathway， its pathological role in the development and progression of MAFLD， and the current intervention strategies targeting this mechanism， in order to provide a theoretical basis for analyzing the pathogenesis of MAFLD and developing novel therapeutic strategies.
