ArticleFrontiers in pharmacology2024
Rabeprazole suppressed gastric intestinal metaplasia through activation of GPX4-mediated ferroptosis.
Article in Frontiers in pharmacology, 2024. 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.
- Rabeprazole attenuates fibrosis by modulating SMAD3 linker region phosphorylation.Biomedical reports · 2026Article
- Targeting ferroptosis inInternational journal of oncology · 2026Review
- Mechanistic insights into the hepatoprotective role of rabeprazole against cyclophosphamide-induced hepatotoxicity via AMPK/SIRT1 activation and suppression of TLR4/NF-κB and MAPK pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- miR-136: A biomarker in the inflammation-cancer transformation of gastric cancer.World journal of gastrointestinal oncology · 2025Article
- Spasmolytic Polypeptide-Expressing Metaplasia in Chronic Atrophic Gastritis and Its Role in the Progression From Gastritis to Gastric Cancer.Journal of digestive diseasesReview
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Authors and funding
12 authors.
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Abstract
Background: Gastric intestinal metaplasia is a common pathological feature in patients with Methods: Real-time PCR, Western blotting (WB) and ROS analysis were conducted to confirm that rabeprazole could induce ferroptosis to suppress gastric intestinal metaplasia. Cellular fraction, luciferase and chromatin immunoprecipitation (ChIP) were used to identify the mechanism underlying rabeprazole modulated ferroptosis. Results: Herein, we found rabeprazole treatment led to inhibit CDX2 and MUC2 expression, alleviating gastric intestinal metaplasia, which was attributed to enhanced ferroptosis characterized by decreased GPX4 expression. Inhibition of ferroptosis by ferrostatin-1 (Fer-1) could reverse decreased CDX2 and MUC2 expression caused by rabeprazole. Mechanically, Rabeprazole could inhibit CREB phosphorylation and nuclear translocation, which further decreased the binding of CREB to GPX4 promoter, reducing GPX4 transactivity. Moreover, endogenous PKA interacted with CREB, and this interaction was drastically destroyed in response to rabeprazole treatment. Most importantly, enhanced ferroptosis was observed in Conclusion: These findings suggested that rabeprazole induced ferroptosis to reduce CDX2 expression in gastric epithelial cells through PKA/CREB cascade signaling, implying that targeting ferroptosis could be a promising strategy in improving gastric intestinal metaplasia during
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