ArticleScientific reports2017
Myeloid differentiation primary response gene (MyD) 88 signalling is not essential for intestinal fibrosis development.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed.
- Intestinal Fibrosis in Inflammatory Bowel Disease and the Prospects of Mesenchymal Stem Cell Therapy.Frontiers in immunology · 2022Review
- How to place the duality of specific MMP-9 inhibition for treatment of inflammatory bowel diseases into clinical opportunities?Frontiers in immunology · 2022Review
- The Oxysterol Synthesising Enzyme CH25H Contributes to the Development of Intestinal Fibrosis.Journal of Crohn's & colitis · 2019Article
- Severity of local inflammation does not impact development of fibrosis in mouse models of intestinal fibrosis.Scientific reports · 2018Article
- Review
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dysregulation of the immune response to microbiota is associated with inflammatory bowel disease (IBD), which can trigger intestinal fibrosis. MyD88 is a key component of microbiota signalling but its influence on intestinal fibrosis has not been clarified. Small bowel resections from donor-mice were transplanted subcutaneously into the neck of recipients C57BL/6 B6-MyD88tm1 Aki (MyD88
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Registered trials
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