ArticleMolecular medicine (Cambridge, Mass.)2025
Hyperoxia-activated Nrf2 regulates ferroptosis in intestinal epithelial cells and intervenes in inflammatory reaction through COX-2/PGE2/EP2 pathway.
Article in Molecular medicine (Cambridge, Mass.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Ellagic Acid Enhances RSL3-Induced Ferroptosis by Inhibiting the Nrf2/HO-1 Signaling Pathway in Pancreatic Ductal Adenocarcinoma.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Arctic Fox-DerivedLife (Basel, Switzerland) · 2026Article
- Neonatal Quercetin Reduces Intestinal Oxidative Damage and Upregulates Tight Junction-Related Genes in a Mouse Experimental Model of Cerebral Palsy.Antioxidants (Basel, Switzerland) · 2026Article
- Oocyte aging in focus: Environmental and endogenous stressors driving reproductive potential decline.GeroScience · 2026Review
- Evaluation of Antioxidant and Anti-Inflammatory Effects of a Nanoformulation Derived from Annurca Apple Callus Extract in an In Vitro Model of Iron Overload-Induced Inflammation.Antioxidants (Basel, Switzerland) · 2025Article
- Disorders of Iron Metabolism: A "Sharp Edge" of Deoxynivalenol-Induced Hepatotoxicity.Metabolites · 2025Article
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Authors and funding
6 authors.
Funding
Abstract
The lack of knowledge about the mechanism of hyperoxia-induced intestinal injury has attracted considerable attention, due to the potential for this condition to cause neonatal complications. This study aimed to explore the relationship between hyperoxia-induced oxidative damage and ferroptosis in intestinal tissue and investigate the mechanism by which hyperoxia regulates inflammation through ferroptosis. The study systematically evaluated the effects of hyperoxia on oxidative stress, mitochondrial damage, ferroptosis, and inflammation of intestinal epithelial cells both in vitro and in vivo. The results showed that ferroptosis was involved in intestinal oxidative damage caused by hyperoxia and was regulated by Nrf2. Moreover, hyperoxia-induced oxidative damage regulated inflammation through ferroptosis by upregulating the COX-2/PGE2/EP2 signaling pathway. These findings have important implications for future clinical prevention and therapeutic approaches to neonatal organ injury caused by hyperoxia treatment.
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