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Ferroptosis plays a novel role in nonalcoholic steatohepatitis pathogenesis

Affiliation
Department of Gastroenterology ,Sichuan Academy of Medical Science and Sichuan Provincial People’s Hospital ,Chengdu ,China
Xiong, Fei;
Affiliation
Department of Rheumatology and Immunology ,Sichuan Academy of Medical Science and Sichuan Provincial People’s Hospital ,Chengdu ,China
Zhou, Qiao;
Affiliation
Department of Critical Care Medicine ,Sichuan Academy of Medical Science and Sichuan Provincial People’s Hospital ,University of Electronic Science and Technology of China ,Chengdu ,China
Huang, Xiaobo;
Affiliation
Department of Pharmacy ,Union Hospital ,Tongji Medical College ,Huazhong University of Science and Technology ,Wuhan ,China
Cao, Peng;
Affiliation
Department of Critical Care Medicine ,Sichuan Academy of Medical Science and Sichuan Provincial People’s Hospital ,University of Electronic Science and Technology of China ,Chengdu ,China
Wang, Yi

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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License Holder: Copyright © 2022 Xiong, Zhou, Huang, Cao and Wang.

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