期刊
FRONTIERS IN PHARMACOLOGY
卷 13, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fphar.2022.1055793
关键词
ferroptosis; dihydroorotate dehydrogenase; mitochondrial glutathione; NASH; mitochondria
资金
- National Natural Science Foundation of China [81802504, 81872207, 81903901]
- Sichuan Science and Technology Bureau [2019YFS0439, 2020JDJQ0067, 2020JDRC0118, 2021YJ0564, 2022YFH0005]
- Science and Technology Innovation Project of Chengdu, China [2021YF05-00225-SN]
- Sichuan Medical Association [Q19037]
- Sichuan Provincial Health Commission [20PJ105]
This article summarizes the role of ferroptosis in the pathogenesis of nonalcoholic steatohepatitis (NASH) and discusses the relationship between ferroptosis, mitochondrial dysfunction, and NASH. Potential pharmacological therapies targeting ferroptosis in NASH are also proposed.
Ferroptosis relies on iron, and ferroptotic cell death is triggered when the balance of the oxidation-reduction system is disrupted by excessive lipid peroxide accumulation. A close relationship between ferroptosis and nonalcoholic steatohepatitis (NASH) is formed by phospholipid peroxidation substrates, bioactive iron, and reactive oxygen species (ROS) neutralization systems. Recent studies into ferroptosis during NASH development might reveal NASH pathogenesis and drug targets. Our review summarizes NASH pathogenesis from the perspective of ferroptosis mechanisms. Further, we discuss the relationship between mitochondrial dysfunction, ferroptosis, and NASH. Finally, potential pharmacological therapies directed to ferroptosis in NASH are hypothesized.
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