铁死亡在非酒精性脂肪性肝炎发病机制中发挥着新作用。
Ferroptosis plays a novel role in nonalcoholic steatohepatitis pathogenesis.
作者信息
Xiong Fei, Zhou Qiao, Huang Xiaobo, Cao Peng, Wang Yi
机构信息
Department of Gastroenterology, Sichuan Academy of Medical Science and Sichuan Provincial People's Hospital, Chengdu, China.
Department of Rheumatology and Immunology, Sichuan Academy of Medical Science and Sichuan Provincial People's Hospital, Chengdu, China.
出版信息
Front Pharmacol. 2022 Dec 2;13:1055793. doi: 10.3389/fphar.2022.1055793. eCollection 2022.
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.
铁死亡依赖于铁，当氧化还原系统的平衡因过量脂质过氧化物积累而被破坏时，就会引发铁死亡性细胞死亡。磷脂过氧化底物、生物活性铁和活性氧（ROS）中和系统在铁死亡与非酒精性脂肪性肝炎（NASH）之间形成了密切关系。最近对NASH发展过程中铁死亡的研究可能揭示NASH的发病机制和药物靶点。我们的综述从铁死亡机制的角度总结了NASH的发病机制。此外，我们还讨论了线粒体功能障碍、铁死亡与NASH之间的关系。最后，推测了针对NASH中铁死亡的潜在药物治疗方法。
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