ArticleBMC medicine2025
Gut microbiota-derived glutathione from metformin treatment alleviates intestinal ferroptosis induced by ischemia/reperfusion.
Article in BMC medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Unveiling the miR‑26a‑5p/MSMO1/7‑DHC Axis: A Novel Therapeutic Target in Myocardial Ischemia-Reperfusion Injury.Cardiovascular drugs and therapy · 2026Article
- Metformin as a Multifaceted Therapeutic Agent for Gastrointestinal Diseases: Mechanisms, Clinical Efficacy, and Future Directions.Pharmacology research & perspectives · 2026Review
- Hypoxia synergizes cGAS-STING activation and AKT1 phosphorylation to drive pulmonary inflammation in one-lung ventilation: therapeutic attenuation by RU.521 and MK2206.Journal of inflammation (London, England) · 2026Article
- The Effects of Reduced Glutathione on Growth Performance, Intestinal Inflammation, and Gut Microbiota in Immune-Stressed Broiler Chickens.Animals : an open access journal from MDPI · 2026Article
- Intestinal Ischemia/Reperfusion Injury: Mechanisms, Diagnosis, and Therapeutic Advances.International journal of biological sciences · 2026Review
- Astaxanthin Alleviates Intestinal Ferroptosis through Gut CommensalResearch (Washington, D.C.) · 2026Article
- Pharmacological strategies for intestinal ischemia-reperfusion injury: mechanisms and therapeutic advances.Frontiers in pharmacology · 2026Review
- Crosstalk Between Microbiome and Ferroptosis in Diseases: From Mechanism to Therapy.Comprehensive Physiology · 2025Review
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Authors and funding
12 authors.
Funding
Abstract
backgroundIntestinal ischemia/reperfusion injury (IIRI) is a life-threatening condition caused by multiple organ and system failures induced by dysbiosis and gut leakage. Metformin has demonstrated efficacy in protecting against IIRI, although the precise role of the gut microbiota in the underlying mechanism is still ambiguous.
methodsThis study examined intestinal barrier function and ferroptosis-related parameters in mice with IIRI following treatment with metformin. Additionally, dirty cages and antibiotics were utilized to investigate the impact of the microbiota on the effects of metformin. The analysis included an assessment of the microbial composition of metformin-treated mice and the biosynthetic activity of specific metabolites.
resultsMetformin effectively reduced gut leakage induced by IIRI, as evidenced by decreased intestinal permeability and increased Occludin, ZO-1, Claudin-1, and MUC-1 expression. A decrease in the expression of the pro-ferroptotic proteins ACSL4, TFR1, and VDAC2/3 and a decrease in dihydroethidium (DHE) fluorescence, iron, malondialdehyde (MDA), and myeloperoxidase (MPO) were further observed in metformin-treated mice. In contrast, the damage to the GPX4/GSH system caused by IIRI was reversed after metformin treatment, as shown by increases in GPX4, SLC7A11, and GSH. The antiferroptotic effects of metformin were phenocopied by its fecal microbiota but were eliminated by antibiotic intake. 16S rRNA analysis revealed that the metformin-modulated gut microbiota was characterized by increased Lactobacillus murinus, which expressed higher levels of GshF that contributed to the mitigation of IIRI.
conclusionsMurine gut microbiota mediated the anti-ferroptotic effect of metformin on IIRI, and the resulting increase in microbial GSH synthesis could serve as a critical pathway for anti-IIRI.
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