ArticleFrontiers in immunology2025
Penicillamine ameliorates intestinal barrier damage in dextran sulfate sodium-induced experimental colitis mice by inhibiting cuproptosis.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- From copper imbalance to immunometabolic remodeling: cuproptosis-related vulnerability and therapeutic hypotheses in autoimmune diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Machine learning-based identification of a metabolic cell death gene signature for assessing disease activity and immunological landscape in inflammatory bowel disease.Scientific reports · 2026Article
- Cuproptosis: Biomarkers, Mechanisms and Treatments in Diseases.Molecules (Basel, Switzerland) · 2026Review
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Authors and funding
8 authors.
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Abstract
Background: Cuproptosis is a copper-dependent form of cell death. However, its role in ulcerative colitis (UC) remains unknown. Aim: To investigate whether cuproptosis is involved in UC and whether penicillamine (PA) improves colitis in mice by inhibiting cuproptosis. Methods: We analyzed the expression of cuproptosis-related genes in patients with UC using the Gene Expression Omnibus database. We used dextran sulfate sodium (DSS) to establish an experimental model of UC and explore the effects of cuproptosis on the intestinal barrier. Mice were treated with the copper-depleting agent tetrathiomolybdate to establish causality between cuproptosis and intestinal barrier damage in mice with DSS-induced colitis. We assessed the effects of PA on the intestinal barrier in mice with DSS-induced colitis. Key methodologies included copper quantification using inductively coupled plasma mass spectrometry and rubeanic acid histochemical staining, along with the analysis of cuproptosis-related and barrier proteins using qRT-PCR, immunoblotting, immunohistochemistry, and immunofluorescence. Results: Cuproptosis was closely related to intestinal barrier damage in patients with UC and in DSS-induced colitis mice, characterized by increased copper levels and dihydrolipoamide S-acetyltransferase (DLAT) oligomerization and reduced Fe-S cluster-containing proteins ferredoxin 1 (FDX1) and lipoyl synthase (LIAS) levels. Copper depletion ameliorated disease-related manifestations in mice with colitis, mitigated the aberrant expression of pro-inflammatory factors, and concurrently enhanced the expression of tight junction proteins. PA inhibited cuproptosis in the intestinal barrier of mice with colitis by reducing excess copper levels and DLAT oligomerization, as well as rescuing the loss of FDX1 and LIAS. Conclusion: Cuproptosis is involved in UC pathogenesis. The identification of PA, which inhibits cuproptosis in the intestinal barrier of mice with colitis, provides a novel therapeutic option for the clinical management of UC.
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