ArticleCell death discovery2025
SAA3 deficiency exacerbates intestinal fibrosis in DSS-induced IBD mouse model.
Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
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Who cites it
3 citing papers in PubMed.
- Enhancing glioma immunotherapy by disrupting RBP-J-mediated NNMT signaling in tumor microenvironment.Oncogene · 2026Article
- Research status and molecular mechanisms of disulfidptosis in cardiovascular diseases (Review).Molecular medicine reports · 2026Review
- Intestinal epithelial AhR deletion aggravates DSS-induced colitis via lipid- and amino-acid metabolic reprogramming: integrated metabolomic-transcriptomic evidence.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Intestinal fibrosis, as a late-stage complication of inflammatory bowel disease (IBD), leads to bowel obstruction and requires surgical intervention, significantly lowering the quality of life of affected patients. SAA3, a highly conserved member of the serum amyloid A (SAA) apolipoprotein family in mice, is synthesized primarily as an acute phase reactant in response to infection, inflammation and trauma. An increasing number of evidence suggests that SAA3 exerts a vital role in the fibrotic process, even though the underlying mechanisms are not yet fully comprehended. This study utilized dextran sulfate sodium (DSS) to establish an IBD mouse model and observed that the SAA3-deficient mice exhibited more severe intestinal fibrosis. Our results further indicated that SAA3 genetic disruption in fibroblasts enhanced cell activation to myofibroblasts through HSPB1/NF-κB/TGF-β1/Smads signaling cascade, exacerbating the pathological phenotype of intestinal fibrosis. Collectively, our results shed novel lights on regulating SAA3 in intestinal fibrosis and indicate the potential to develop therapeutic strategies for IBD patients.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.