ArticleInternational endodontic journal2025
EZH2 knockout in mice activates STAT3 signalling via STAT3 methylation and modulates ferroptosis in pulpitis-affected dental pulp vascular endothelial cells: A laboratory investigation.
Article in International endodontic journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The trial behind it
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Who cites it
7 citing papers in PubMed.
- Epigenetic and post-translational regulatory networks of ferroptosis in the tumor immune microenvironment.Experimental hematology & oncology · 2026Review
- An Exploration of Nanobiotechnology Bridging Patho-Therapeutics with Regenerative and Clinical Perspectives in Periodontitis.Journal of functional biomaterials · 2026Review
- EZH2-Mediated Epigenetic Modifications Induce Pyroptosis in Dental Pulp Endothelial Cells via Activation of NLRP6 Inflammasome During Pulpitis Development.Mediators of inflammation · 2026Article
- Immune cells dying from ferroptosis: mechanisms and therapeutic opportunities.Cell death & disease · 2025Review
- Review
- EZH2 knockout in mice activates STAT3 signalling via STAT3 methylation and modulates ferroptosis in pulpitis-affected dental pulp vascular endothelial cells: A laboratory investigation.International endodontic journal · 2025Article
- Fibroblasts-specific p16Clinical and translational medicine · 2025Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
aimRecent findings suggest that mitigating ferroptosis could serve as an effective strategy for treating inflammation. This study aimed to investigate the role that the enhancer of zeste homologue 2 (EZH2) mediated the signal transducer and activator of transcription 3 (stat3) methylation plays in the modulation of ferroptosis in pulpitis. The study results offer potential advancements in the therapeutic approaches for pulpitis and provide new insights and strategies for managing this condition. METHODOLOGY: Bioinformatics analysis combined with methylation capture sequencing of EZH2
resultsBioinformatics analysis identified a link between pulpitis and DNA methylation. Methylation sequencing further revealed the association of methylation with ferroptosis and the regulation of STAT3 methylation by EZH2. In vitro, lipopolysaccharide (LPS) stimulation induced ferroptosis, whereas EZH2 disruption suppressed STAT3 expression but increased Glutathione Peroxidase 4 (GPX4) expression, leading to the escalation of oxidative stress and exacerbation of ferroptosis. This illustrates the complex interactions between methylation, ferroptosis and oral inflammation, highlighting potential therapeutic targets.
conclusionsOverall, pulpitis plays a crucial role in EZH2-mediated STAT3 methylation and activates ferroptosis by regulating GPX4 expression. This study provides new insights and strategies for treatment and advances our understanding of the pathogenesis of pulpitis.
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Registered trials
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