ArticleJournal of orthopaedic translation2026
HIF1A transcriptionally activates CDKN1A to drive ferroptosis in skeletal muscle ischaemia-reperfusion injury.
Article in Journal of orthopaedic translation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Ferroptosis in skeletal muscle: from molecular mechanisms to therapeutic interventions.Journal of orthopaedic translation · 2026Review
- Integrating mechanistic research and emerging technologies to advance clinical translation in orthopaedics.Journal of orthopaedic translation · 2026Article
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Authors and funding
13 authors.
Funding
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Abstract
Background: Skeletal muscle ischaemia-reperfusion (I/R) injury involves complex redox dysregulation with limited treatments. Although ferroptosis contributes to other organ I/R injuries, its role and regulation in skeletal muscle remain unclear. This study aimed to investigate the role and regulatory mechanism of ferroptosis in skeletal muscle I/R injury, specifically focusing on whether hypoxia-inducible factor 1 alpha (HIF1A) transcriptionally activates cyclin-dependent kinase inhibitor 1a (CDKN1A/p21) to drive this process. Methods: We employed integrative transcriptomics and Cleavage Under Targets and Tagmentation (CUT&Tag, a chromatin mapping technique) sequencing in murine I/R models. Genetic inhibition ( Results: HIF1A directly bound to the Conclusion: Our findings establish HIF1A as a context-dependent ferroptosis amplifier in skeletal muscle I/R injury, acting through direct transcriptional activation of The Translational Potential of this Article: Targeting the HIF1A-CDKN1A axis offers a promising therapeutic approach to reduce skeletal muscle damage and improve clinical outcomes after ischaemia-reperfusion injury.
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Registered trials
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