ArticleGastroenterology research and practice2026
Identification of TIMP1 as a Key Regulator of Ferroptosis in Ulcerative Colitis Through Bioinformatics and Functional Experiments.
Article in Gastroenterology research and practice, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Identification of TIMP1 as a Key Regulator of Ferroptosis in Ulcerative Colitis Through Bioinformatics and Functional Experiments.Gastroenterology research and practice · 2026Article
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Authors and funding
4 authors.
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Abstract
Background: Ferroptosis is an iron-dependent form of regulated cell death, whereas the precise mechanism of ferroptosis in the pathogenesis of ulcerative colitis (UC) remains to be elucidated. The tissue inhibitor Metalloproteinase 1 (TIMP1) is involved in ferroptosis of UC, whereas its regulatory function remains unclear. This study is aimed at exploring the potential effect on ferroptosis in UC. Methods: Gene expression profiling data of colonic biopsies from UC patients and healthy controls were acquired from the GSE87466 dataset. The expression of TIMP1, GPX4, and SLC7A11 was determined using western blot. The mRNA levels of TIMP1, PGRMC1, IL-1 Results: Bioinformatics identified TIMP1 and PGRMC1 as core genes related to ferroptosis of UC. Both TIMP1 and PGRMC1 were upregulated in colonic biopsies from UC patients in the GSE87466 dataset. The mRNA expression was induced after LPS treatment, whereas PGRMC1 was not significantly altered. TIMP1 knockdown inhibited the expression of IL-1 Conclusion: TIMP1 regulated ferroptosis, inflammatory response, and intestinal epithelial permeability in LPS-induced intestinal epithelial cells, suggesting TIMP1 as a potential therapeutic target for UC.
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