ArticleScientific reports2025
CGRPβ suppresses the pathogenesis of ulcerative colitis via the immunoproteasome.
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 2 papers.
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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
2 citing papers in PubMed.
- Review
- Enteric glia, neuropeptides, and Parkinson's: impacts of calcitonin gene-related peptide on gut alpha synuclein.American journal of physiology. Gastrointestinal and liver physiology · 2026Article
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Authors and funding
8 authors.
Funding
Abstract
Various factors have been implicated in the pathogenesis of ulcerative colitis (UC), with immune system failure being the most important one. Calcitonin gene-related peptide (CGRP), a neuropeptide with two isoforms, CGRPα and CGRPβ, has been reported to regulate the immune system. In this study, we investigated the role of CGRP isoforms in UC pathogenesis. We induced UC-like symptoms in CGRPα and CGRPβ knockout (KO) mice using dextran sulphate sodium. Compared to wild-type and CGRPα KO mice, CGRPβ-deficient mice exhibited severe symptoms with increased blood in the stool and diarrhoea. Proteome analysis revealed significant up-regulation of immune-related proteins and immunoproteasome components in CGRPβ-deficient mice, suggesting that an enhanced immune response contributes to the severity of this disease. Treatment with ONX-0914, an immunoproteasome inhibitor, markedly improved these symptoms, highlighting the role of the immunoproteasome in exacerbating UC. This study provides the first evidence that CGRPβ protects against UC by modulating immune responses, particularly those mediated by the immunoproteasome. Our findings suggest that functional differences in CGRP isoforms may influence the severity and management of UC. This insight into the neuro-immune mechanism of UC opens avenues for novel therapies that address both the neural and immune aspects of this disease.
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