ArticleJournal of cardiovascular translational research2025
Hypoxia Aggravates Myocardial Ischemia/Reperfusion Injury Through the Promotion of Ferroptosis via ACSL4 Lactylation.
Article in Journal of cardiovascular translational research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The trial behind it
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Who cites it
8 citing papers in PubMed.
- Lactylation: Metabolic epigenetic regulation and cell death mechanisms in myocardial ischemia‒reperfusion injury.Genes & diseases · 2027Review
- Potential Relationship Between Ferroptosis and Pyroptosis in Myocardial Ischemia/Reperfusion Injury: Molecular Mechanisms and Therapeutic Targets.Reviews in cardiovascular medicine · 2026Review
- Lactylation-regulated ferroptosis: mechanisms, disease associations, and therapeutic strategies.Archives of pharmacal research · 2026Review
- Lipocalin 2: a double-edged sword in cellular ferroptosis.Cell biology and toxicology · 2026Review
- Progress of Research on the Metabolic Regulation of Lactylation in Muscle Tissues and Its Disease Associations.Biomolecules · 2026Review
- Epigenetic and post-translational regulatory networks of ferroptosis in the tumor immune microenvironment.Experimental hematology & oncology · 2026Review
- The immune-cardiovascular metabolic circuitry in myocardial ischemia-reperfusion injury: from metabolic signal release to spatiotemporal reprogramming.Frontiers in immunology · 2026Review
- Review
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocardial ischemia/reperfusion injury (MIRI) worsens ischemic damage, with ferroptosis as a key mediator of this iron-dependent cell death. Lactylation, a novel epigenetic modification, remains poorly understood in MIRI-associated ferroptosis. This study aimed to elucidate the mechanistic link between lactylation and ferroptosis in MIRI. Experimental results demonstrated that hypoxia/reoxygenation (H/R) induction combined with lactate (LA) treatment significantly enhanced the protein expression levels, lactylation status, and protein stability of acyl-CoA synthetase long-chain family member 4 (ACSL4). Site-specific analysis identified lysine 83 (K83) as the critical lactylation modification site on ACSL4. Functional studies revealed that LDHA knockdown-mediated suppression of lactate levels attenuated ferroptosis in H/R-treated cells, an effect that was reversed by ACSL4 overexpression. In vivo validation confirmed that LDHA depletion ameliorated ferroptosis-related damage and mitigated MIRI-induced cardiac dysfunction. Collectively, these findings establish that lactylation-regulated ACSL4 ferroptosis exacerbates MIRI pathogenesis, suggesting that targeting the lactylation-ACSL4 axis represents a promising therapeutic strategy for MIRI.
Indexed as
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.