ArticleJournal of inflammation research2024
Estrogen Receptor β Alleviates Colitis by Inhibiting Ferroptosis in Intestinal Epithelial Cells.
Article in Journal of inflammation research, 2024. 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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Who cites it
8 citing papers in PubMed.
- Fibroblast-specificAmerican journal of physiology. Gastrointestinal and liver physiology · 2026Article
- The role of estrogen and its receptors in the regulation of ferroptosis and autophagy.Molecular biology reports · 2026Review
- NCOA4-mediated ferritinophagy modulates colitis-associated ferroptosis in intestinal epithelial cells and mucosal repair.Biology direct · 2026Article
- Rethinking estrogen receptor β in EAOC: a synergistic modulator in a genomically informed landscape.Journal of ovarian research · 2026Review
- From gut-reproductive microbiota to ferroptosis: a comprehensive insight into the molecular-pathogenicity of endometriosis.Frontiers in immunology · 2026Review
- Article
- Epigenomic Profiling Positions ATF7 as a Core Regulator of Colonic Inflammation.Journal of cellular and molecular medicine · 2025Article
- Mechanisms of Magnoliae Officinalis Cortex Volatile Oil in Alleviating 5-Fluorouracil-Induced Mucositis via Multi-Omics Approaches.Drug design, development and therapy · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Ulcerative colitis (UC), a major type of inflammatory bowel disease, is characterized by chronic inflammation of the colonic mucosa and submucosa. Estrogen receptor β (ERβ) predominates in the colon and exerts anti-inflammatory effects. Ferroptosis, a recently discovered form of iron-dependent programmed cell death, is implicated in the pathogenesis of several diseases, including UC. However, the link between ferroptosis and the anti-inflammatory actions of ERβ in UC remains to be elucidated. Methods: We analyzed colonic mucosal samples from inflammatory and non-inflammatory regions of UC patients to assess ferroptosis levels. Experimental colitis was induced in wild-type C57BL/6 mice and intestinal epithelial cell-specific ERβ knockout (ERβ Results: In UC patients, ferroptosis was significantly elevated in inflammatory mucosal regions compared to non-inflammatory areas. Compared to the wild-type counterparts, ERβ Conclusion: Our findings demonstrate that ERβ deficiency exacerbates colitis and enhances ferroptosis in IECs. ERβ positively regulates GPX4 transcription, thereby inhibiting ferroptosis and alleviating colitis. These insights suggest that modulation of ERβ and its regulation of ferroptosis may represent a novel therapeutic strategy for UC.
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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.