FGF21 maintains redox homeostasis and promotes neuronal survival after traumatic brain injury by targeting SLC25A39-mediated mitochondrial GSH transport
Our findings provide preliminary evidence that FGF21 confers protective effects against mitochondrial oxidative stress-related damage following TBI. Additionally, we elucidated a novel role for SLC25A39-dependent mitochondrial GSH transport in both the pathological processes subsequent to TBI and the physiological functions of FGF21.
Authors
- Yuan Ma (ORCID: https://orcid.org/0000-0003-4311-7105)
- Jianing Luo
- L Wang
- Heng Guo (ORCID: https://orcid.org/0000-0002-5252-5015)
- Qing Ouyang (ORCID: https://orcid.org/0000-0001-8729-1290)
- T. Yang (ORCID: https://orcid.org/0009-0000-7217-3304)
- Weiwei Li (ORCID: https://orcid.org/0000-0003-3485-164X)
- Bing Sun (ORCID: https://orcid.org/0000-0002-1992-3767)
- Xun Wu (ORCID: https://orcid.org/0000-0002-8213-3178)
Institutions
- Chengdu Military General Hospital (CN)
- Air Force Medical University (CN)
Publication Details
- Journal
- Journal of Translational Medicine
- Published
- 2025-10-02
- DOI
- https://doi.org/10.1186/s12967-025-06969-3
- Citations
- 4
- Primary Topic
- Fibroblast Growth Factor Research
- Type
- article
- Field-Weighted Citation Impact
- 3.22