GPX4
脂质过氧化
程序性细胞死亡
辅酶Q10
生物化学
化学
谷胱甘肽
细胞生物学
生物
氧化应激
酶
谷胱甘肽过氧化物酶
细胞凋亡
作者
Yulei Song,Hong-Xu Lei,Dou Yu,He Zhu,Meng-Zhu Hao,Ronghua Cui,Xiang-Shuai Meng,X. D. Sheng,Lei Zhang
出处
期刊:Biofactors
[Wiley]
日期:2023-12-07
卷期号:50 (2): 266-293
被引量:1
摘要
Ferroptosis is a new form of regulated cell death caused by iron-dependent accumulation of lethal polyunsaturated phospholipids peroxidation. It has received considerable attention owing to its putative involvement in a wide range of pathophysiological processes such as organ injury, cardiac ischemia/reperfusion, degenerative disease and its prevalence in plants, invertebrates, yeasts, bacteria, and archaea. To counter ferroptosis, living organisms have evolved a myriad of intrinsic efficient defense systems, such as cyst(e)ine-glutathione-glutathione peroxidase 4 system (cyst(e)ine-GPX4 system), guanosine triphosphate cyclohydrolase 1/tetrahydrobiopterin (BH4) system (GCH1/BH4 system), ferroptosis suppressor protein 1/coenzyme Q10 system (FSP1/CoQ10 system), and so forth. Among these, GPX4 serves as the only enzymatic protection system through the reduction of lipid hydroperoxides, while other defense systems ultimately rely on small compounds to scavenge lipid radicals and prevent ferroptotic cell death. In this article, we systematically summarize the chemical biology of lipid radical trapping process by endogenous chemicals, such as coenzyme Q10 (CoQ10), BH4, hydropersulfides, vitamin K, vitamin E, 7-dehydrocholesterol, with the aim of guiding the discovery of novel ferroptosis inhibitors.
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