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ISSN 1001-5256 (Print)
ISSN 2097-3497 (Online)
CN 22-1108/R
Volume 42 Issue 8
Aug.  2026
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Article Contents

Role of innate immune mechanisms triggered by mitochondrial DNA release in metabolic dysfunction-associated fatty liver disease and targeted intervention strategies

DOI: 10.12449/JCH260832
Research funding:

National Natural Science Foundation of China (82160866);

Science and Technology Planning Project of Guizhou Province (Qiankehe Jichu-ZK[2023]General 433);

Traditional Chinese Medicine and Ethnic Medicine Science and Technology Research Project of Guizhou Province (QZYY-2025-182)

More Information
  • Corresponding author: Yang Mei, 908417289@qq.com (ORCID: 0009-0003-3563-4767)
  • Received Date: 2025-12-22
  • Accepted Date: 2026-01-12
  • Published Date: 2026-08-25
  • 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.

     

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