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Ferroptosis and Neurodegenerative Diseases: Insights into the Regulatory Roles of SLC7A11

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Abstract

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.

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Funding

This work was supported by National Natural Science Foundation of China (No. 81502779), and Natural Science Foundation of Liaoning province, China (No. QN2019030).

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All authors contributed to the conception and preparation of the manuscript. The manuscript was written by CW and all authors commented on previous versions of the manuscript. All authors read and approved the final manuscript.

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Correspondence to Wei Liu.

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Wang, C., Liu, H., Xu, S. et al. Ferroptosis and Neurodegenerative Diseases: Insights into the Regulatory Roles of SLC7A11. Cell Mol Neurobiol 43, 2627–2642 (2023). https://doi.org/10.1007/s10571-023-01343-7

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  • DOI: https://doi.org/10.1007/s10571-023-01343-7

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