ArticleJournal of gastroenterology2026
METTL3/YTHDF1 drives M1 macrophage polarization and aggravates ulcerative colitis progression by regulating m6A modification of SerpinB5 mRNA and FBXO32-dependent NF-κB pathway.
Article in Journal of gastroenterology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 2 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.
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Who cites it
2 citing papers in PubMed.
- FBXO11 and FBXO32 synergistically activate innate immunity against hepatitis B virus in a NEDD8-dependent manner.Frontiers in immunology · 2026Article
- Macrophage dysregulation in inflammatory bowel disease: cellular heterogeneity, pathogenic mechanism, and treatment.Frontiers in immunology · 2026Review
Corrections and comments
- Erratum issued
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundUlcerative colitis (UC) is an idiopathic chronic intestinal inflammation. It has been reported that macrophages are key cells mediating inflammation. Furthermore, Serpin family B member 5 (SerpinB5) plays a role in the regulation of macrophage phenotype conversion. However, the role and underlying mechanism of SerpinB5 in UC are still unclear.
methodsHematoxylin and eosin staining assay was used to assess colon pathological changes. GO enrichment and KEGG pathway enrichment analyses were conducted to assess the function of the DEGs from RNA-seq data. GSE224758 database, RNA-seq, and GeneCards database were applied to analyze the intersection targets. The mRNA and protein levels of the related genes were determined using RT-qPCR and western blot. The in vitro model of UC was established by stimulating colonic epithelial cells with tumor necrosis factor α (TNF-α). Cell viability, proliferation, and apoptosis were determined using CCK-8, EdU, and flow cytometry. Senescence-associated β-galactosidase (SA-β-Gal) staining and senescence-related proteins p53 and p16 were detected to evaluate the endothelial cell senescence. Inflammatory cytokines and oxidative stress were detected using ELISA and kits. Flow cytometry analysis assessed the percentage of CD11b
resultsSerpinB5 expression was increased in UC patients, TNF-α-treated FUC cells, and a mouse model of UC. SerpinB5 silencing repressed TNF-α-induced cell apoptosis, cell senescence, inflammation response, oxidative stress, and M1 macrophage polarization. Meanwhile, SerpinB5 knockdown relieved symptoms of the mouse model of UC and repressed M1 macrophage polarization. SerpinB5 positively mediated the NF-κB pathway by regulating FBXO32. METTL3 improved the stability of SerpinB5 mRNA in an m6A-YTHDF1-dependent manner.
conclusionMETTL3/YTHDF1 aggravated UC progression through promoting M1 macrophage polarization via SerpinB5 mRNA m6A modification and FBXO32/NF-κB pathway. These findings indicated that SerpinB5 might be a good and promising therapeutic target for UC treatment.
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Registered trials
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