ArticleCell biology and toxicology2025
DNMT1 recruits RUNX1 and represses FOXO1 transcription to inhibit anti-inflammatory activity of regulatory T cells and augments sepsis-induced lung injury.
Article in Cell biology and toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- RUNX3: a regulator of macrophage apoptosis with positive prognostic impact in sepsis.Genes & genomics · 2026Article
- SKP2 Regulates Pulmonary Inflammatory Injury Triggered by Bacterial Infection Through p27-Mediated Degradation of FOXN3.MedComm · 2026Article
- Review
- The regulation of oxidative stress response by epigenetic modifications in acute respiratory distress syndrome.Journal of thoracic disease · 2026Review
- The Dual Role of RUNX1 in Inflammation-Driven Age-Related Diseases: From Molecular Mechanisms to Clinical Translation.Biomedicines · 2025Review
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Authors and funding
6 authors.
Funding
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Abstract
Sepsis-induced lung injury (ALI) is a critical condition characterized by excessive immune responses and tissue damage. Previous evidence has underscored an upregulation pattern of DNA methyltransferase 1 (DNMT1) in sepsis. This study reveals the key role of DNMT1 in modulating regulatory T cell (Treg) activity in septic ALI. A septic mouse model was generated through cecal ligation and puncture. Treatment with either DNMT1 antagonist Thioguanine (ThG) or AAV-sh-DNMT1 significantly reduced immune cell infiltration, reduced production of pro-inflammatory cytokines, and increasing production of anti-inflammatory cytokines in the bronchoalveolar lavage fluid (BALF) of mice, alongside improved lung pathology and integrity. Furthermore, the DNMT1 inhibition or silencing significantly enhanced population of FOXP3
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