ArticleClinical epigenetics2025
EZH1 deficiency promotes ferroptosis resistance by activating NRF2 in sepsis-associated liver injury.
Article in Clinical epigenetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Histone Post-Translational Modifications Regulating Ferroptosis: The Molecular Mechanisms and Disease Associations.Cell biochemistry and function · 2026Review
- EZH1 Inhibition attenuates apoptosis and promotes regeneration for liver repair in acute liver failure.BMC gastroenterology · 2025Article
- The emerging role of ferroptosis in the pathological development and progression of sepsis.Military Medical Research · 2025Review
- Ferroptosis and Metabolic Dysregulation: Emerging Chemical Targets in Cancer and Infection.Molecules (Basel, Switzerland) · 2025Review
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5 authors.
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Abstract
Sepsis-associated acute liver injury (SALI) is a major clinical complication of sepsis due to excessive, unfettered inflammation. In recent years, the role of epigenetic regulatory mechanisms in SALI has been gradually emphasized. Here, we investigated the effects of a Histone-lysine N-methyltransferase EZH1 (Enhancer of zeste homolog 1) inhibition on promoting ferroptosis resistance to activate nuclear factor, erythroid derived 2, like 2 (NRF2) in SALI. We found that EZH1 deficiency improved animal survival in lethal sepsis. EZH1 deficiency mice exhibited alleviated SALI with decreased hepatocellular ferroptosis. EZH1 deficiency attenuated the H3K27me3 modification in the Nfe2l2 promoter, lending to the increased expression and nuclear translocation of NRF2. In the in vitro, LPS-induced ferroptosis model, EZH1 inhibitor DS3201 exhibited an anti-ferroptosis effect, which was reversed NRF2 inhibitor ML385. These findings indicate that EZH1 deficiency or inhibition with DS3201 alleviates ferroptosis in the liver by activating the NRF2, and it is suggested that targeting EZH1 may be a new therapeutic strategy in SALI.
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