Review Advance Articles
Role of mitochondrial quality control in the pathogenesis of nonalcoholic fatty liver disease
- 1 Department of Clinical Laboratory Medicine, The First Medical Center, Chinese PLA General Hospital, Beijing 100853, China
- 2 Department of Chemical Engineering, University of Minnesota-Duluth, Duluth, MN 55812, USA
- 3 Medical School of Chinese PLA, Chinese PLA General Hospital, Beijing 100853, China
received: October 22, 2019 ; accepted: March 19, 2020 ; published: March 26, 2020 ;https://doi.org/10.18632/aging.102972
How to Cite
Copyright © 2020 Li et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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.