ArticleJournal of clinical and translational hepatology2024
GPX4 Promoter Hypermethylation Induced by Ischemia/Reperfusion Injury Regulates Hepatocytic Ferroptosis.
Article in Journal of clinical and translational hepatology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Preconditioning with sufentanil confers protective effects in transplantation by attenuating hepatic ischemia-reperfusion injury.World journal of transplantation · 2026Review
- Galectin-3 Promotes Graft Injury via NLRP3 Pyroptosis in Steatotic Liver Transplantation: A Therapeutic Target for Donor Optimization.Journal of clinical and translational hepatology · 2026Article
- Tacrolimus (FK506) Attenuates Hepatic Ischemia-Reperfusion Injury via Oxidative Glutathione Metabolism and Suppression of Lipoxygenase-Mediated Cell Death.Antioxidants (Basel, Switzerland) · 2026Article
- Targeting Autophagy, Ferroptosis, and Neuroinflammation: Polyphenol-Mediated Modulation of Emerging Signaling Pathways in Neurodegeneration.Molecular neurobiology · 2026Review
- Bimodal regulation and precision therapy of neutrophil extracellular traps in liver ischemia-reperfusion injury: recent advances.Frontiers in immunology · 2026Review
- Exploring cell death mechanisms in liver transplantation: implications for graft survival.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background and Aims: Glutathione peroxidase 4 (GPX4) is a key factor in ferroptosis, which is involved in ischemia-reperfusion injury. However, little is known about its role in hepatic ischemia-reperfusion injury (HIRI). This study aimed to investigate the role of GPX4 methylation in ferroptosis during HIRI. Methods: For the Results: Ferroptosis was observed in oxygen and glucose deprivation, characterized by a significant decrease in cellular viability ( Conclusions: Ferroptosis may be the primary mode of cell death in hepatocytes following ischemia-reperfusion injury. The methylation of the
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