ArticleBrain and behavior2026
ETV4 Improves Cerebral Ischemia-Reperfusion Injury by Restraining YBX1-GPX4-Ferroptosis Cascades.
Article in Brain and behavior, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundCerebral ischemia-reperfusion injury (CIRI) is a critical pathological process following ischemic stroke, with ferroptosis being increasingly recognized as a key contributor to neuronal damage. However, the regulatory mechanisms, particularly the role of specific transcription factors like E26 transformation-specific variant 4 (ETV4), remain poorly understood. This study aimed to investigate the function and underlying mechanism of ETV4 in neuronal ferroptosis during CIRI.
methodsIn vitro, SH-SY5Y cells subjected to oxygen-glucose deprivation/reoxygenation (OGD/R) were used to model CIRI. Cell viability and ferroptosis markers (Fe
resultsETV4 was significantly down regulated in both the MCAO/R model and OGD/R-treated cells. Overexpression of ETV4 markedly attenuated OGD/R-induced oxidative stress, ferroptosis in vitro, and ameliorated brain injury in vivo. Mechanistically, ETV4 transcriptionally activated YBX1 by directly binding to its promoter. YBX1, in turn, stabilized GPX4 mRNA, which was modified by NSUN2-mediated methylation. Crucially, the protective effects of ETV4 in vitro were abolished upon YBX1 or GPX4 knockdown.
conclusionOur findings demonstrate that ETV4 transcriptionally up regulates YBX1 to stabilize GPX4 mRNA in an NSUN2-m5Cmethylation dependent manner, thus suppressing neuronal ferroptosis. This reveals a novel ETV4/YBX1/GPX4 axis as a potential therapeutic target for CIRI.
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