ArticleEuropean journal of medical research2025
TLR4/NF-κB-mediated M1 macrophage polarization contributes to the promotive effects of ETS2 on ulcerative colitis.
Article in European journal of medical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Elevation of liver elasticity following radiofrequency ablation reflects neutrophil-mediated abscopal effect in liver cancer.JHEP reports : innovation in hepatology · 2026Article
- Aqueous Extract ofVeterinary sciences · 2026Article
- Lipoteichoic Acid Stimulation of Macrophages Causes Mitochondrial Dysfunction.International dental journal · 2026Article
- Emerging Nanomaterials Can Even Treat Chronic Wounds: A Review of Evidence on Magnesium-Based Systems.International journal of nanomedicine · 2026Review
- Macrophage dysregulation in inflammatory bowel disease: cellular heterogeneity, pathogenic mechanism, and treatment.Frontiers in immunology · 2026Review
- Research Progress on the Relationship Between the Intestinal Barrier and Macrophages.Current issues in molecular biology · 2025Review
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Authors and funding
5 authors.
Funding
Abstract
objectiveETS2 is a core modulator of macrophages. This study aims to investigate the effects of ETS2 on macrophage polarization in ulcerative colitis (UC) and the involvement of TLR4/NF-κB pathway.
methodsA dextran sulfate sodium (DSS)-induced acute UC mice model was established, along with a lipopolysaccharide (LPS)/IFN-γ-stimulated RAW264.7 cell model to mimic inflammation. Immunofluorescence was employed to examine the co-localization of ETS2 with M1 macrophage markers (F4/80 and iNOS). Flow cytometry quantified the iNOS
resultsIn DSS-induced UC mice, ETS2 was significantly upregulated in colon tissues and co-localized with F4/80. LPS/IFN-γ-treated RAW264.7 cells also exhibited elevated ETS2 expression, accompanied by increased inflammatory cytokine secretion, expansion of iNOS
conclusionETS2 enhanced the inflammatory response in UC by activating TLR4/NF-κB-mediated M1 macrophage polarization.
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