ArticleImmunity, inflammation and disease2025
C9orf72 Alleviates DSS‑Induced Ulcerative Colitis via the cGAS-STING Pathway.
Article in Immunity, inflammation and disease, 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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Who cites it
4 citing papers in PubMed.
- The Role of cGAS-STING-Driven PANoptosis in Neurodegenerative Diseases and Therapeutic Prospects.Cells · 2026Review
- Mitophagy-related molecular signatures in ulcerative colitis revealed by machine learning and molecular dynamics.Frontiers in genetics · 2026Article
- Molecular Subtypes and Biomarkers of Ulcerative Colitis Revealed by Sphingolipid Metabolism-Related Genes: Insights from Machine Learning and Molecular Dynamics.Current issues in molecular biology · 2025Article
- Identifying Lactylation-related biomarkers and therapeutic drugs in ulcerative colitis: insights from machine learning and molecular docking.BMC pharmacology & toxicology · 2025Article
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3 authors.
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Abstract
purposeC9orf72 deficiency contributes to severe inflammation in mice. Ulcerative colitis (UC) is a chronic inflammatory disorder with the shortage of clinical success. However, whether C9orf72 is involved in the progression of UC is not fully understood. This study investigated whether C9orf72 could alleviate dextran sulfate sodium (DSS)-induced colitis in mice and lipopolysaccharide (LPS)-induced colitis in Caco-2 cells.
methodsMice were injected AAV9-C9orf72 lentivirus through tail vein and fed 3% DSS for a week. Caco-2 cells were cultured to establish C9orf723 overexpressed model. Histopathological examination, level of inflammation, cGAS-STING pathway, and gut barrier function were detected in mice and cells.
resultsC9orf72 overexpression in mice attenuated DSS-induced colitis and intestinal epithelial barrier damage by stimulating ZO-1 and Occludin expression. In LPS-induced Caco-2 cells, C9orf72 overexpression increased cell viability and the expression of ZO-1 and Occludin. C9orf72 overexpression alleviated inflammation by inhibiting the cGAS-STING pathway in colonic tissue and Caco-2 cells.
conclusionC9orf72 overexpression attenuated DSS-induced colitis and intestinal epithelial barrier damage by inhibiting the cGAS-STING pathway. C9orf72 may present a target for mitigating UC.
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