ArticleRedox biology2025
GAMG alleviates liver fibrosis through inducing ferroptosis in inflammatory macrophages via the IRF1/SLC7A11 signaling pathway.
Article in Redox biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Breaking the cycle of fibrosis: Ferroptosis as a therapeutic target (Review).International journal of molecular medicine · 2026Review
- METTL3/FTO drives ferroptosis in colorectal cancer by targeting mJournal of gastroenterology · 2026Article
- Glucose starvation induces fumarate hydratase succinylation and inhibits ferroptosis to maintain colon cancer cell proliferation.Cell death & disease · 2026Article
- Engineered polypeptide cascade-release platform restores macrophage plasticity for accelerated diabetic wound healing.Bioactive materials · 2026Article
- H3K9 acetylation-dependent CHAC1 transcription in dihydroartemisinin-induced hepatic stellate cell ferroptosis.Chinese medical journal · 2026Article
- A novel role of the TNF-α/p65/IRF1 axis in aggravating rheumatoid arthritis through the induction of fibroblast-like synoviocytes pyroptosis.Frontiers in pharmacology · 2026Article
- Dual Roles of Natural Products in Regulating Ferroptosis in Acute and Chronic Liver Diseases: A Review.Oxidative medicine and cellular longevity · 2026Review
- Ginsenoside Rg1 antagonizes diabetic osteoporosis by regulating ferroptosis via mitochondrial membrane potential in H-type vascular endothelial cells.Frontiers in aging · 2026Article
- Myeloid cells in chronic liver inflammation.Cellular & molecular immunology · 2025Review
- SLC7A11 in Fibrosis: Molecular Mechanisms and Future Prospects.Aging and disease · 2025Review
- Macrophage heterogeneity in liver fibrosis.Frontiers in immunology · 2025Review
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11 authors.
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Abstract
The activation of inflammatory macrophages plays a pivotal role in the development of liver fibrosis (LF). Ferroptosis contributes to the clearance of inflammatory macrophages and the release of profibrotic factors. Glycyrrhetic Acid 3-O-Mono-β-d-glucuronide (GAMG) is a natural compound, the potential role of which on LF remains uncertain. In this study, GAMG treatment significantly reduced hepatocyte steatosis, fibroplasia, inflammatory cell infiltration, and collagen fiber deposition in LF mice. In addition, GAMG remarkably decreased the content of collagen protein and improved liver function indicators. Single-cell RNA sequencing revealed that GAMG significantly affected the changes of macrophage subsets in LF, and Funrich analysis identified IRF1 as a key transcription factor regulating the macrophage genome. IRF1 was significantly increased while ferroptosis related SLC7A11 was significantly down-regulated in GAMG treated inflammatory macrophages. Mass spectrometry metabolomics analysis showed that GAMG significantly affected metabolites associated with LF. In vivo and in vitro experiments further verified that GAMG induced ferroptosis of inflammatory macrophages through the IRF1/SLC7A11 axis, and ultimately alleviated LF. Therefore, GAMG induces ferroptosis of inflammatory macrophages by activating the IRF1/SLC7A11 axis, which provides a new strategy for the treatment of LF.
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