ArticleFrontiers in immunology2022
Increased stromal PFKFB3-mediated glycolysis in inflammatory bowel disease contributes to intestinal inflammation.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 31 citations in OpenAlex.
- Multi-Omics and Machine Learning-Based Characterization of the Lactylation Microenvironment and Biomarker Identification in Crohn's Disease Intestinal Fibrosis.International journal of molecular sciences · 2026Article
- From inflammation to malignancy: the dynamic evolution of cancer-associated fibroblasts in IBD-CRC.Neoplasia (New York, N.Y.) · 2026Review
- Targeting Glycolytic Metabolism in Cancer Therapy: Current Approaches and Future Perspectives.Cells · 2026Review
- FGF 13 functions as a regulator of the ERK/aerobic glycolysis axis in the inflammatory state during septic lung injury.Nature communications · 2026Article
- Selective autophagic degradation of glycolytic activator PFKFB3 contributes to maintaining intestinal epithelial barrier in inflammatory bowel disease.International journal of molecular medicine · 2026Article
- Inhibition of PFKFB3 in macrophages ameliorates intestinal inflammation by modulating gut microbiota in DSS-induced colitis.mSystems · 2026Article
- Immune and metabolic remodeling following bariatric surgery: Implications for targeted immunotherapy (Review).International journal of molecular medicine · 2026Review
- Roles of immune cell metabolism in rheumatoid arthritis.Frontiers in immunology · 2026Review
- β-arrestin2: an emerging player and potential therapeutic target in inflammatory immune diseases.Acta pharmacologica Sinica · 2025Review
- Stromal Cell Subsets Show Model-Dependent Changes in Experimental Colitis and Affect Epithelial Tissue Repair and Immune Cell Activation.Inflammatory bowel diseases · 2025Article
- SAA3 deficiency exacerbates intestinal fibrosis in DSS-induced IBD mouse model.Cell death discovery · 2025Article
- PFKFB3 alleviates the advancement ofFrontiers in cellular and infection microbiology · 2025Article
- SMRT-depleted conventional DCs maintain inflammation despite lower glycolysis via mTOR signalling and succinate oxidation.npj metabolic health and disease · 2024Article
- Advances in the understanding of the role and mechanism of action of PFKFB3‑mediated glycolysis in liver fibrosis (Review).International journal of molecular medicine · 2024Review
- Metabolic regulation of the immune system in health and diseases: mechanisms and interventions.Signal transduction and targeted therapy · 2024Review
- Colonic Dysregulation of Major Metabolic Pathways in Experimental Ulcerative Colitis.Metabolites · 2024Article
- The Impact of Glycolysis and Its Inhibitors on the Immune Response to Inflammation and Autoimmunity.Molecules (Basel, Switzerland) · 2024Review
- Pathogenic role of PFKFB3 in endothelial inflammatory diseases.Frontiers in molecular biosciences · 2024Review
- Emerging Role of Plant-Based Dietary Components in Post-Translational Modifications Associated with Colorectal Cancer.Life (Basel, Switzerland) · 2023Review
- Senescent melanocytes driven by glycolytic changes are characterized by melanosome transport dysfunction.Theranostics · 2023Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammatory bowel disease (IBD) is a chronic relapsing inflammation of the intestinal tract with currently not well-understood pathogenesis. In addition to the involvement of immune cells, increasing studies show an important role for fibroblasts in the pathogenesis of IBD. Previous work showed that glycolysis is the preferred energy source for fibroblasts in fibrotic diseases. 6-phosphofructo-2-kinase/fructose-2, 6-bisphosphatase 3 (PFKFB3) is a key kinase supporting glycolysis. Increased expression of PFKFB3 in several cancers and inflammatory diseases has been previously reported, but the metabolic status of fibroblasts and the role of PFKFB3 in patients with IBD are currently unknown. Therefore, in this study, we evaluated the role of glycolysis and PFKFB3 expression in IBD. Single-sample gene set enrichment analysis (ssGSEA) revealed that glycolysis was significantly higher in IBD intestinal samples, compared to healthy controls, which was confirmed in the validation cohorts of IBD patients. Single-cell sequencing data indicated that PFKFB3 expression was higher in IBD-derived stromal cells.
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