ArticlePloS one2023
Glycolytic reprogramming is involved in tissue remodeling on chronic rhinosinusitis.
Article in PloS one, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 7 citations in OpenAlex.
- Diagnostic value and immune microenvironment regulatory network of metabolic reprogramming in chronic rhinosinusitis with nasal polyps identified by multidimensional transcriptome integration and machine learning.Frontiers in immunology · 2026Article
- Aquaporin-1 upregulation is associated with scleral remodeling during myopia development in mice.American journal of translational research · 2026Article
- Development and internal validation of a nomogram and machine-learning models for postoperative recurrence in adult patients with chronic rhinosinusitis with nasal polyps.Frontiers in medicine · 2026Article
- Dysregulated glycosaminoglycan biosynthesis and retinoid metabolism in chronic rhinosinusitis with nasal polyps: insights from a comprehensive transcriptomic analysis.Frontiers in immunology · 2026Article
- Hypoxia: a critical pathophysiological driver in respiratory inflammatory diseases.Military Medical Research · 2026Review
- IRF4 Knockdown Inhibits the Chronic Rhinosinusitis Without Nasal Polyps Development by Regulating NLRP3/Caspase-1/GSDMD-Mediated Pyroptosis.Biochemical genetics · 2025Article
- Article
- NFκB and JNK pathways mediate metabolic adaptation upon ESCRT-I deficiency.Cellular and molecular life sciences : CMLS · 2024Article
- Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGlycolytic reprogramming is a key feature of chronic inflammatory disease. Extracellular matrix (ECM) produced by myofibroblasts plays an important role in tissue remodeling of nasal mucosa in chronic rhinosinusitis (CRS). This study aimed to determine whether glycolytic reprogramming contributes to myofibroblast differentiation and ECM production in nasal fibroblasts.
methodsPrimary nasal fibroblasts were isolated from the nasal mucosa of patients with CRS. Glycolytic reprogramming was assessed by measuring the extracellular acidification and oxygen consumption rates in nasal fibroblast, with and without transforming growth factor beta 1 (TGF-β1) treatment. Expression of glycolytic enzymes and ECM components was measured by real-time polymerase chain reaction, western blotting, and immunocytochemical staining. Gene set enrichment analysis was performed using whole RNA-sequencing data of nasal mucosa of healthy donors and patients with CRS.
resultGlycolysis of nasal fibroblasts stimulated with TGF-B1 was upregulated along with glycolytic enzymes. Hypoxia-inducing factor (HIF)-1α was a high-level regulator of glycolysis, and increased HIF-1α expression promoted glycolysis of nasal fibroblasts, and inhibition of HIF-1α down-regulated myofibroblasts differentiation and ECM production.
conclusionThis study suggests that inhibition of the glycolytic enzyme and HIF-1α in nasal fibroblasts regulates myofibroblast differentiation and ECM generation associated with nasal mucosa remodeling.
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