ArticleNPJ biofilms and microbiomes2025
TSP50 deficiency in neural stem cells aggravates colitis in mice by altering intestinal microbiome.
Article in NPJ biofilms and microbiomes, 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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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
3 citing papers in PubMed.
- Optimized protocols for culturing and sectioning mouse intestinal organoids: enhancing efficiency and structural integrity.MethodsX · 2026Article
- TSP50 attenuates metabolic dysfunction-associated steatotic liver disease via SCD1 degradation-mediated suppression of hepatocyte lipogenesis.Cellular & molecular biology letters · 2026Article
- Depression and anxiety in inflammatory bowel disease: mechanisms and emerging therapeutics targeting the microbiota-gut-brain axis.Frontiers in immunology · 2025Review
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Authors and funding
20 authors.
Funding
Abstract
Inflammatory bowel disease (IBD) is a complex disease characterized by persistent chronic inflammation of the gastrointestinal tract and periodic episodes. Despite the increasing number of related studies, the detailed pathogenesis of IBD has not been elucidated. In recent years, host-microbiota interactions in the pathogenesis of IBD have received extensive attention. Testes-specific protease 50 (TSP50) is a potential risk gene for IBD, but whether it can affect the susceptibility of colitis by regulating the gut microbiome is still unclear. Here, we showed that TSP50 deficiency in neural stem cells (NSCs) aggravated colitis in mice by altering intestinal microbiome. Mechanistically, TSP50 maintained the level of neurotransmitter acetylcholine (ACh) by degrading acetylcholinesterase (AChE), thereby maintaining intestinal mucosa and intestinal microecological homeostasis and reducing the susceptibility to colitis. These findings provide a new perspective on the interaction between host and commensal microbiota, which may be beneficial for developing potential therapeutic strategies for IBD.
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Registered trials
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