Molecular regulatory mechanism of the SIRT2/NF-κB p65 signaling pathway in ferroptosis-promoted spinal cord injury repair
In summary, these findings indicate that SIRT2 overexpression can suppress ferroptosis through NF-κB p65 deacetylation, facilitating SCI repair. Therefore, a deeper understanding of the interaction between SIRT2 and NF-κB p65 and their roles in the regulation of ferroptosis is of paramount importance for developing novel therapeutic approaches for spinal cord injury.
Authors
- Changsheng Gong
- Zetian Zhao
- Yu Zhou (ORCID: https://orcid.org/0000-0002-9731-9362)
- Shengbo Shi (ORCID: https://orcid.org/0000-0002-1849-7292)
- Tienan Wang
- Meng Zhang
- Xingxing Huang (ORCID: https://orcid.org/0000-0002-7333-8454)
- Xiaobing Yu (ORCID: https://orcid.org/0000-0002-3318-1720)
- Junxiao Gao (ORCID: https://orcid.org/0000-0002-5333-3816)
- Zijing Zhang (ORCID: https://orcid.org/0000-0001-7470-0307)
- Pengpeng Shi (ORCID: https://orcid.org/0000-0001-8329-809X)
Institutions
- Shangqiu First People's Hospital (CN)
- Affiliated Zhongshan Hospital of Dalian University (CN)
Publication Details
- Journal
- BMC Neurology
- Published
- 2025-11-12
- DOI
- https://doi.org/10.1186/s12883-025-04164-x
- Primary Topic
- Ferroptosis and cancer prognosis
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- Dalian Science and Technology Innovation Fund