Role of mitochondrial quality control in the pathogenesis of nonalcoholic fatty liver disease

Ruibing Li, Sam Toan, Hao Zhou

Research output: Contribution to journalArticlepeer-review

10 Scopus citations


Nutrient oversupply and mitochondrial dysfunction play central roles in nonalcoholic fatty liver disease (NAFLD). The mitochondria are the major sites of β-oxidation, a catabolic process by which fatty acids are broken down. The mitochondrial quality control (MQC) system includes mitochondrial fission, fusion, mitophagy and mitochondrial redox regulation, and is essential for the maintenance of the functionality and structural integrity of the mitochondria. Excessive and uncontrolled production of reactive oxygen species (ROS) in the mitochondria damages mitochondrial components, including membranes, proteins and mitochondrial DNA (mtDNA), and triggers the mitochondrial pathway of apoptosis. The functionality of some damaged mitochondria can be restored by fusion with normally functioning mitochondria, but when severely damaged, mitochondria are segregated from the remaining functional mitochondrial network through fission and are eventually degraded via mitochondrial autophagy, also called as mitophagy. In this review, we describe the functions and mechanisms of mitochondrial fission, fusion, oxidative stress and mitophagy in the development and progression of NAFLD.

Original languageEnglish (US)
Pages (from-to)6467-6485
Number of pages19
Issue number7
StatePublished - Apr 15 2020
Externally publishedYes

Bibliographical note

Funding Information:
This work was supported by funds from the China Postdoctoral Science Foundation (Grant No. 2019TQ0128) and the National Science Foundation of China (Grant Nos. 81900252, 81770261, 81900254 and 91749128).


  • Fission
  • Fusion
  • Mitochondrial quality control
  • Mitophagy

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