ArticleActa pharmaceutica Sinica. B2024
Hyperglycemia activates FGFR1
Article in Acta pharmaceutica Sinica. B, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 10 citations in OpenAlex.
- Cadmium impairs heart ventricular formation and disrupts polysialylated-NCAM/FGF receptor signaling in Xenopus tadpoles.Cell & bioscience · 2026Article
- Gestational diabetes: from pathogenesis to therapeutic intervention.Diabetology & metabolic syndrome · 2026Review
- Shared molecular mechanisms of vascular endothelial cells in psoriasis and diabetes comorbidity.Postepy dermatologii i alergologii · 2026Article
- Unraveling the FGFR-RNA splicing axis: Mechanisms, oncogenic crosstalks and innovations for therapeutic purpose.Acta pharmaceutica Sinica. B · 2026Review
- Role of Innate Immune Receptors in Cardiac Damage Linked to Metabolic Disorders.Handbook of experimental pharmacology · 2026Review
- Regulated Cell Death and Inflammatory Signaling in Diabetic Cardiomyopathy: Mechanisms and Therapeutic Strategies.Journal of cardiovascular translational research · 2025Review
- Therapeutic potential of calcitriol in cerebral ischemia/reperfusion injury: In vivo and in silico insights into TLR4 and FGFR2 pathways.IBRO neuroscience reports · 2025Article
- Gut Microbiota-Derived Metabolites Orchestrate Metabolic Reprogramming in Diabetic Cardiomyopathy: Mechanisms and Therapeutic Frontiers.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Review
- Melatonin receptor 1a alleviates sleep fragmentation-aggravated testicular injury in T2DM by suppression of TAB1/TAK1 complex through FGFR1.Acta pharmaceutica Sinica. B · 2025Article
- Macrophage OTUD1-CARD9 axis drives isoproterenol-induced inflammatory heart remodelling.Clinical and translational medicine · 2024Article
- Fibroblast growth factor signaling in macrophage polarization: impact on health and diseases.Frontiers in immunology · 2024Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Protein tyrosine kinases (RTKs) modulate a wide range of pathophysiological events in several non-malignant disorders, including diabetic complications. To find new targets driving the development of diabetic cardiomyopathy (DCM), we profiled an RTKs phosphorylation array in diabetic mouse hearts and identified increased phosphorylated fibroblast growth factor receptor 1 (p-FGFR1) levels in cardiomyocytes, indicating that FGFR1 may contribute to the pathogenesis of DCM. Using primary cardiomyocytes and H9C2 cell lines, we discovered that high-concentration glucose (HG) transactivates FGFR1 kinase domain through toll-like receptor 4 (TLR4) and c-Src, independent of FGF ligands. Knocking down the levels of either TLR4 or c-Src prevents HG-activated FGFR1 in cardiomyocytes. RNA-sequencing analysis indicates that the elevated FGFR1 activity induces pro-inflammatory responses
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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.