Journal
OPEN MEDICINE
Volume 16, Issue 1, Pages 1718-1727Publisher
DE GRUYTER POLAND SP Z O O
DOI: 10.1515/med-2021-0394
Keywords
liver fibrosis; hepatic stellate cell; ubiquinone; PINK1 mitophagy
Categories
Funding
- National Natural Science Foundation of China [81770601]
- Key Research and Development Program of Hebei Province [182777117D]
- Medical Science Research of Hebei Province [20200058]
Ask authors/readers for more resources
MitoQ inhibits HSC activation and alleviates hepatic fibrosis by enhancing PINK1/parkin-mediated mitophagy.
Mitophagy affects the activation of hepatic stellate cells (HSCs). Mitochondria-targeted ubiquinone (MitoQ) is a mitochondria-targeted antioxidant that reduces the production of intracellular reactive oxygen species (ROS). However, its relationship with mitophagy remains unclear. This study evaluated mitophagy during HSC activation and the effects of MitoQ on mitophagy in cell culture and in an animal model of the activation of HSCs. We found that MitoQ reduced the activation of HSCs and alleviated hepatic fibrosis. PINK1 (PTEN-induced putative kinase 1) is a putative serine/threonine kinase located in the mitochondria's outer membrane. While the activation of primary HSCs or LX-2 cells was associated with reduced PINK1/parkinmediated mitophagy, MitoQ reduced intracellular ROS levels, enhanced PINK1/parkin-mediated mitophagy, and inhibited the activation of HSCs. After knocking down the key mitophagy-related protein, PINK1, in LX-2 cells to block mitophagy, MitoQ intervention failed to inhibit HSC activation. Our results showed that MitoQ inhibited the activation of HSCs and alleviated hepatic fibrosis by enhancing PINK1/parkin-mediated mitophagy.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available