Authors
Kaimin Zeng, Jing-Jing Peng, Ziwei Lan, Da Gao, Pei Zhu, Zihao Zhu, Yan Li
Published in
Free radical research. Pages 1-46. Oct 13, 2026. Epub Oct 13, 2026.
Abstract
Ferroptosis impairs neurological function in ischemic stroke (IS). This study elucidated the mechanism by which Tripartite motif 25 (TRIM25) promotes neuronal ferroptosis during IS.
CCK-8 detected cell viability. Flow cytometry and corresponding kits quantified ferroptosis-related parameters. TTC staining determined cerebral infarct volume. Neurological impairment was assessed using neurological deficit scoring and Nissl staining. RT-qPCR, Western blot, and immunohistochemistry assessed the mRNA and protein expression. Co-IP analyzed the ubiquitinated level of Y-box binding protein 1 (YBX1) and the interaction between TRIM25 and YBX1. ChIP assessed the binding of YBX1 and H3K4me1 at the Ferritin heavy chain 1 (FTH1) promoter. Peptide pull-down assessed the interaction between YBX1 and H3K4me1.
TRIM25 promoted neuronal ferroptosis in IS. TRIM25 promoted YBX1 ubiquitination and degradation. YBX1 knockdown counteracted the suppressive outcome of TRIM25 depletion on OGD/R-induced ferroptosis. YBX1 upregulated FTH1 by recognizing H3K4me1 enrichment at the FTH1 promoter, thus inhibiting OGD/R-induced neuronal ferroptosis. In vivo, TRIM25 knockdown attenuated MCAO/R-induced brain injury via YBX1 upregulation.
TRIM25 induces YBX1 ubiquitination and degradation, impairing YBX1-dependent H3K4me1 enrichment at the FTH1 promoter to downregulate FTH1, thereby promoting neuronal ferroptosis in IS.
PMID:
42867392
Bibliographic data and abstract were imported from PubMed on 14 Oct 2026.
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