ArticleCell death discovery2025
IFN-γ could induce ferroptosis in keloid fibroblasts by inhibiting the expression of serpine2.
Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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Who cites it
3 citing papers in PubMed.
- ATM inhibition restores IFN-γ sensitivity and induces ferroptosis in NSCLC via DNA damage response.Biochemistry and biophysics reports · 2026Article
- Metabolic reprogramming and ferroptosis in keloid pathogenesis: new insights for targeted therapy.Molecular biology reports · 2026Review
- Ferroptosis-related gene analysis revealing novel biomarkers and therapeutic targets in diffuse large B-cell lymphoma.Scientific reports · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Keloids are common pathological scars resulting from previous trauma or inflammation. Interferon-gamma (IFN-γ) has shown significant therapeutic effects when used alone or in combination with other agents. While IFN-γ has been found to regulate ferroptosis in tumor cells, its ability to regulate ferroptosis in keloid fibroblasts (KFs) is unclear. Here, we have demonstrated a direct causal relationship between IFN-γ levels and ferroptosis in KFs. To explore the intrinsic mechanism, we performed genome-wide RNA and proteomics sequencing and found that serpine2 was the most significantly downregulated gene in KFs after exogenous overexpression of IFN-γ. Serpine2, which belongs to a family of serine protease inhibitors, has been shown to play an important role in fibrotic diseases. Therefore, we hypothesized that serpine2 is a downstream gene in the regulation of ferroptosis in KFs by IFN-γ. Our results showed that serpine2 overexpression promotes collagen synthesis, which in turn promotes the proliferation, migration, and invasive functions of KFs. We further demonstrated that serpine2 overexpression promoted system Xc
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Registered trials
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