ArticleFrontiers in immunology2025
Exosomes secreted by ATF3/Nrf2-mediated ferroptotic renal tubular epithelial cells promote M1/M2 ratio imbalance inducing renal interstitial fibrosis following ischemia and reperfusion injury.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Breaking the cycle of fibrosis: Ferroptosis as a therapeutic target (Review).International journal of molecular medicine · 2026Review
- Histone deacetylase 3‑mediated histone deacetylation combined with activating transcription factor 3 promotes renal fibrosis by inhibiting Klotho.Molecular medicine reports · 2026Article
- The ATF3-DRP1 Axis Coordinates Mitochondrial Homeostasis and Suppresses Early Apoptosis in Zinc-Deficient Cardiomyocytes.Biological trace element research · 2026Article
- Activating transcription factors: Orchestrators of macrophage biology in pathological settings (Review).International journal of molecular medicine · 2026Review
- Global trends and emerging hotspots of macrophage research in kidney transplantation: a bibliometric and visualization analysis.Frontiers in immunology · 2026Review
- Inhibitory effects of herbal monomers on ferroptosis in renal fibrosis: a review and mechanistic study.Frontiers in pharmacology · 2025Review
- Ferroptosis in ischemia-reperfusion injury: molecular mechanisms and therapeutic strategies.American journal of cardiovascular disease · 2025Review
- WTAP modulates macrophage polarization in rheumatoid arthritis by targeting exosomal circ-CBLB via mFrontiers in immunology · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Severe renal ischemia and reperfusion injury (IRI) progresses to renal interstitial fibrosis (RIF) with limited therapeutic strategies. Although ferrptosis and macrophage polarization both play important roles in this model, their specific pathogenesis and interactions have not been elucidated. Therefore, we aimed to explore the mechanisms by which ferrotosis occurs in renal tubular epithelial cells (RTECs) and ferroptotic cell-derived exosomes induce macrophage polarization in IRI-related RIF model. Methods: Result: Compared with the sham group, the IR group showed more severe kidney injury in HE staining, more collagen fibers in Masson staining, and higher α-SMA expression levels in immunohistochemistry. Total iron and MDA content increased while GSH content decreased. The IR group had more significant mitochondrial damage and higher PTGS2 and TFRC mRNA levels than those in the sham group. Compared with the IR group, the above indexes were all alleviated in the IR+Fer-1 or IR+ATF3 Conclusion: ATF3 might accelerate the ferroptosis by inhibiting Nrf2/ARE pathway, and exosomes from ferroptotic cells reduced the M1/M2 macrophage ratio, promoting fibrosis.
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