SAT1 promotes the progression of OA by regulating TRIM33-mediated p53 acetylation to enhance ferroptosis
In summary, our data indicate that SAT1 is a potential key gene in OA, revealing the crucial role of the SAT1-TRIM33-p53 axis in OA pathogenesis. This axis promotes ferroptosis by enhancing p53 acetylation, suggesting that targeting SAT1 may represent a novel therapeutic strategy for improving OA.
Authors
- Jing Jiang (ORCID: https://orcid.org/0000-0001-7549-1164)
- Jiexiang Yang
- Lin Luo
- Jing Wang (ORCID: https://orcid.org/0000-0003-3063-3733)
Institutions
- Southwest Medical University (CN)
- Affiliated Hospital of Southwest Medical University (CN)
Publication Details
- Journal
- PLoS ONE
- Published
- 2025-10-08
- DOI
- https://doi.org/10.1371/journal.pone.0332761
- Citations
- 1
- Primary Topic
- Cancer-related molecular mechanisms research
- Type
- article
- Field-Weighted Citation Impact
- 0.94