ArticleFrontiers in endocrinology2018
FGF23 Induction of O-Linked N-Acetylglucosamine Regulates IL-6 Secretion in Human Bronchial Epithelial Cells.
Article in Frontiers in endocrinology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 38 citations in OpenAlex.
- The Interplay Between Obesity and Type 2 Diabetes: Common Pathophysiological Mechanisms Contributing to Telomere Shortening.Life (Basel, Switzerland) · 2025Review
- Identifying KL-6-Associated Immune Cell Signatures and Key Genes in Emphysematous COPD.Journal of inflammation research · 2025Article
- Relationships of serum FGF23 and α-klotho with atherosclerosis in patients with type 2 diabetes mellitus.Cardiovascular diabetology · 2024Article
- O-GlcNAc transferase regulates collagen deposition and fibrosis resolution in idiopathic pulmonary fibrosis.Frontiers in immunology · 2024Article
- Review
- Prednisone-hydrogen sulfide releasing hybrid shows improved therapeutic profile in asthma.Frontiers in pharmacology · 2023Article
- Relationship between serum iPTH and peritonitis episodes in patients undergoing continuous ambulatory peritoneal dialysis.Frontiers in endocrinology · 2023Article
- Receptor tyrosine kinases regulate signal transduction through a liquid-liquid phase separated state.Molecular cell · 2022Article
- Targeting ProteinCells · 2022Review
- O-GlcNAcylation and Its Role in Cancer-Associated Inflammation.Frontiers in immunology · 2022Review
- Regulation of Cr(VI)-Induced Premature Senescence in L02 Hepatocytes by ROS-CaOxidative medicine and cellular longevity · 2022Article
- Modulators of radiation-induced cardiopulmonary toxicities for non-small cell lung cancer: Integrated cytokines, single nucleotide variants, and HBP systems imaging.Frontiers in oncology · 2022Review
- An observational cohort study to assess N-acetylglucosamine for COVID-19 treatment in the inpatient setting.Annals of medicine and surgery (2012) · 2021Article
- The Role of O-GlcNAcylation in Immune Cell Activation.Frontiers in endocrinology · 2021Review
- ST6GAL1 and α2-6 Sialylation Regulates IL-6 Expression and Secretion in Chronic Obstructive Pulmonary Disease.Frontiers in immunology · 2021Article
- Diabetes enhances translation ofThe Journal of biological chemistry · 2020Article
- OGT-Mediated KEAP1 Glycosylation Accelerates NRF2 Degradation Leading to High Phosphate-Induced Vascular Calcification in Chronic Kidney Disease.Frontiers in physiology · 2020Article
- O-GlcNAcylation in immunity and inflammation: An intricate system (Review).International journal of molecular medicine · 2019Review
- Observational
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
The hexosamine biosynthetic pathway (HBP) generates the substrate for the O-linked β-N-acetylglucosamine (O-GlcNAc) modification of proteins. The HBP also serves as a stress sensor and has been reported to be involved with nuclear factor of activated T-cells (NFAT) activation, which can contribute to multiple cellular processes including cell metabolism, proliferation, and inflammation. In our previously published report, Fibroblast Growth Factor (FGF) 23, an important endocrine pro-inflammatory mediator, was shown to activate the FGFR4/phospholipase Cγ (PLCγ)/nuclear factor of activated T-cells (NFAT) signaling in chronic inflammatory airway diseases such as cystic fibrosis (CF) and chronic obstructive pulmonary disease (COPD). Here, we demonstrate that FGF23 increased the O-GlcNAc modification of proteins in HBECs. Furthermore, the increase in O-GlcNAc levels by FGF23 stimulation resulted in the downstream activation of NFAT and secretion of interleukin-6 (IL-6). Conversely, inhibition of FGF23 signaling and/or O-GlcNAc transferase (OGT)/O-GlcNAc reversed these effects. Collectively, these data suggest that FGF23 induced IL-6 upregulation and secretion is, at least, partially mediated via the activation of the HBP and O-GlcNAc levels in HBECs. These findings identify a novel link whereby FGF23 and the augmentation of O-GlcNAc levels regulate airway inflammation through NFAT activation and IL-6 upregulation in HBECs. The crosstalk between these signaling pathways may contribute to the pathogenesis of chronic inflammatory airway diseases such as COPD and CF as well as metabolic syndromes, including diabetes.
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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.