ArticleScientific reports2025
Disulfidptosis links the pathophysiology of ulcerative colitis and immune infiltration in colon adenocarcinoma.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The trial behind it
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Who cites it
4 citing papers in PubMed.
- Disulfidptosis: Mechanisms, evidence boundaries, and translational opportunities.Redox biology · 2026Review
- The Mechanism and Regulation of Disulfidptosis and Its Role in Disease.Biomedicines · 2026Review
- Thymoquinone and caffeic acid phenethyl ester mitigate experimental ulcerative colitis: a biochemical and histopathological study.Acta cirurgica brasileira · 2026Article
- Advances in novel cell death mechanisms in breast cancer: intersecting perspectives on ferroptosis, cuproptosis, disulfidptosis, and pyroptosis.Molecular cancer · 2025Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Ulcerative colitis (UC), a chronic inflammatory bowel disease, significantly increases the risk of colon adenocarcinoma (COAD). Disulfidptosis, a novel form of programmed cell death, has been implicated in various diseases, including UC. This study investigates the expression of disulfidptosis-related genes, particularly CD2AP and MYH10, in UC and COAD. Through analysis of public datasets, we found MYH10 significantly upregulated and CD2AP downregulated in UC compared to healthy controls, with consistent patterns in COAD. Immune infiltration analysis revealed correlations between these genes and specific immune cell types, suggesting their roles in immune modulation. Molecular docking showed strong binding affinities of UC drugs such as budesonide and sulfasalazine with CD2AP and MYH10. Connectivity Map analysis identified additional drug candidates, including simvastatin and mephenytoin, which may be repurposed for UC and COAD therapy. These findings suggest disulfidptosis-related genes as potential biomarkers and therapeutic targets, linking chronic inflammation to cancer progression.
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Registered trials
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