Wang Chen, Liu Haihui, Xu Si, Deng Yu, Xu Bin, Yang Tianyao, Liu Wei
Department of Environmental Health, School of Public Health, China Medical University, No. 77 Puhe Road, Shenbei New District, Shenyang, 110122, Liaoning, China.
Cell Mol Neurobiol. 2023 Aug;43(6):2627-2642. doi: 10.1007/s10571-023-01343-7. Epub 2023 Mar 29.
Programed cell death plays a key role in promoting human development and maintaining homeostasis. Ferroptosis is a recently identified pattern of programmed cell death that is closely associated with the onset and progression of neurodegenerative diseases. Ferroptosis is mainly caused by the intracellular accumulation of iron-dependent lipid peroxides. The cysteine/glutamate antibody Solute carrier family 7 member 11 (SLC7A11, also known as xCT) functions to import cysteine for glutathione biosynthesis and antioxidant defense. SLC7A11 has a significant impact on ferroptosis, and inhibition of SLC7A11 expression promotes ferroptosis. Moreover, SLC7A11 is also closely associated with neurodegenerative diseases. In this paper, we summarize the relationship between ferroptosis and neurodegenerative diseases and the role of SLC7A11 during this process. The various regulatory mechanisms of SLC7A11 are also discussed. In conclusion, we are looking forward to a theoretical basis for further understanding the occurrence and development of ferroptosis in SLC7A11 and neurodegenerative diseases, and to seek new clues for the treatment of neurodegenerative diseases.
程序性细胞死亡在促进人类发育和维持体内平衡方面发挥着关键作用。铁死亡是最近发现的一种程序性细胞死亡模式,与神经退行性疾病的发生和发展密切相关。铁死亡主要由铁依赖性脂质过氧化物在细胞内积累引起。半胱氨酸/谷氨酸反向转运体溶质载体家族7成员11(SLC7A11,也称为xCT)的功能是导入半胱氨酸用于谷胱甘肽生物合成和抗氧化防御。SLC7A11对铁死亡有重大影响,抑制SLC7A11表达可促进铁死亡。此外,SLC7A11也与神经退行性疾病密切相关。在本文中,我们总结了铁死亡与神经退行性疾病之间的关系以及SLC7A11在此过程中的作用。还讨论了SLC7A11的各种调控机制。总之,我们期待为进一步理解SLC7A11介导的铁死亡及神经退行性疾病的发生发展提供理论依据,并为神经退行性疾病的治疗寻找新线索。