The DOI matches its Crossref record; 47 of the 47 references it cites were found in a registry or an index.
Zinc attenuates ferroptosis and promotes functional recovery in contusion spinal cord injury by activating Nrf2/GPX4 defense pathway
Open accessAbstract
Aim: Spinal cord injury (SCI) involves multiple pathological processes. Ferroptosis has been shown to play a critical role in the injury process. We wanted to explore whether zinc can inhibit ferroptosis, reduce inflammation, and then exert a neuroprotective effect. Methods: The Alice method was used to establish a spinal cord injury model. The Basso Mouse Scale (BMS), Nissl staining, hematoxylin‐eosin staining, and immunofluorescence analysis were used to investigate the protective effect of zinc on neurons on spinal cord neurons and the recovery of motor function. The regulation of the nuclear factor E2/heme oxygenase‐1 (NRF2/HO‐1) pathway was assessed, the levels of essential ferroptosis proteins were measured, and the changes in mitochondria were confirmed by transmission electron microscopy and 5,5′,6,6′‐tetrachloro‐1,1′,3,3′‐tetraethyl‐imidacarbocyanine iodide (JC‐1) staining. In vitro experiments using VSC4.1 (spinal cord anterior horn motor neuroma cell line), 4‐hydroxynonenal (4HNE), reactive oxygen species (ROS), superoxide dismutase (SOD), malondialdehyde (MDA), glutathione (GSH), lipid peroxides, and finally the levels of inflammatory factors were detected to assess the effect of zinc. Results: Zinc reversed behavioral and structural changes after SCI. Zinc increased the expression of NRF2/HO‐1, thereby increasing the content of glutathione peroxidase 4 (GPX4), SOD, and GHS and reducing the levels of lipid peroxides, MDA, and ROS. Zinc also rescued injured mitochondria and effectively reduced spinal cord injury and the levels of inflammatory factors, and the NRF2 inhibitor Brusatol reversed the effects of zinc. Conclusion: Zinc promoted the degradation of oxidative stress products and lipid peroxides through the NRF2/HO‐1 and GPX4 signaling pathways to inhibit ferroptosis in neurons.
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Ferroptosis: An Iron-Dependent Form of Nonapoptotic Cell Death
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The CoQ oxidoreductase FSP1 acts parallel to GPX4 to inhibit ferroptosis
Bersuker, K., Hendricks, J. M., Li, Z., Magtanong, L., Ford, B., Tang, P. H., Roberts, M. A., Tong, B., Maimone, T. J., Zoncu, R., et al. (2019) · Nature · doi:10.1038/s41586-019-1705-2 · Cited by 3,703
The ARRIVE guidelines 2.0: Updated guidelines for reporting animal research
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Regulated necrosis: the expanding network of non-apoptotic cell death pathways
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Selenium Utilization by GPX4 Is Required to Prevent Hydroperoxide-Induced Ferroptosis
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Synchronized renal tubular cell death involves ferroptosis
Linkermann, A., Skouta, R., Himmerkus, N., Mulay, S. R., Dewitz, C., De Zen, F., Prokai, A., Zuchtriegel, G., Krombach, F., Welz, P.-S., et al. (2014) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1415518111 · Cited by 1,126
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Brusatol enhances the efficacy of chemotherapy by inhibiting the Nrf2-mediated defense mechanism
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Cited by
Iron Homeostasis and Ferroptosis in Human Diseases: Mechanisms and Therapeutic Prospects
Ru, Q., Li, Y., Chen, L., Wu, Y., Min, J., & Wang, F. (2024) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-024-01969-z · Cited by 724
Metadata
- Authors
- Ge, M., Tian, H., Mao, L., Li, D., Lin, J., Hu, H., Huang, S., Zhang, C., & Mei, X.
- Venue
- CNS Neuroscience & Therapeutics
- Publisher
- Wiley
- Published
- 2021-05-05
- Volume
- 27
- Issue
- 9
- Pages
- 1023-1040
- ISSN
- 1755-5930 (ISSN-L)
- 1755-5949
- OpenAlex
- W3158010667
- Cited by
- 267
- References
- 47
- FWCI
- 24.22
- Type
- journal article
- Language
- en
- Open access
- gold
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- Ge, M., Tian, H., Mao, L., Li, D., Lin, J., Hu, H., Huang, S., Zhang, C., & Mei, X. (2021). Zinc attenuates ferroptosis and promotes functional recovery in contusion spinal cord injury by activating Nrf2/GPX4 defense pathway. CNS Neuroscience & Therapeutics. https://doi.org/10.1111/cns.13657
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