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Intestinal Epithelial Cell Ferroptosis in Ulcerative Colitis: Pathogenesis, Signaling Networks, and Therapeutic
Zhi-Qiang Zhao1, Zhou-Xin Yu1, Zhi-Qiu Liu1
1Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Current Medical Science
|May 19, 2026
Summary
Ferroptosis, a cell death process involving lipid peroxidation, drives ulcerative colitis (UC). Targeting ferroptosis pathways offers new therapeutic strategies for managing this inflammatory bowel disease.
Area of Science:
- Gastroenterology
- Cell Biology
- Pathophysiology
Background:
- Ferroptosis, an iron-dependent cell death, is implicated in ulcerative colitis (UC) pathogenesis.
- Key features include lipid peroxidation, iron overload, and disrupted antioxidant systems in intestinal epithelial cells (IECs).
Purpose of the Study:
- To review the hallmarks of IEC ferroptosis in UC.
- To describe regulatory signaling networks involved in ferroptosis.
- To evaluate therapeutic strategies targeting ferroptosis in UC.
Main Methods:
- Literature review of ferroptosis mechanisms in UC.
- Analysis of signaling pathways (Nrf2/HO-1, SLC7A11/GPX4, AMPK/mTOR).
- Systematic evaluation of emerging therapeutic interventions.
Main Results:
- IEC ferroptosis is a critical driver of UC.
- Specific signaling pathways regulate ferroptosis in UC.
- Therapeutic strategies include antioxidant activation, metabolism regulation, and immune modulation.
Conclusions:
- Understanding ferroptosis mechanisms in UC is crucial for developing targeted therapies.
- Novel therapeutic paradigms for UC can be developed by targeting ferroptosis.
- Disease-stage-specific treatments for UC can emerge from this research.
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