ArticleJournal of cell communication and signaling2017
Catabolic effects of FGF-1 on chondrocytes and its possible role in osteoarthritis.
Article in Journal of cell communication and signaling, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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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
18 citing papers in PubMed, 32 citations in OpenAlex.
- PIEZO1 variants that reduce open channel probability are associated with familial osteoarthritis.The Journal of biological chemistry · 2026Article
- Multi-Omics Integration Identifies FGF1 as a Diagnostic Biomarker and RAS-MAPK-Driven Pathogenic Factor in Osteoarthritis.Journal of inflammation research · 2025Article
- ELIXCYTECurrent issues in molecular biology · 2024Article
- Role of signaling pathways in age-related orthopedic diseases: focus on the fibroblast growth factor family.Military Medical Research · 2024Review
- Osteoarthritis versus psoriasis arthritis: Physiopathology, cellular signaling, and therapeutic strategies.Genes & diseases · 2024Review
- Analysis of proteins released from osteoarthritic cartilage by compressive loading.Scientific reports · 2023Article
- FGF1 reduces cartilage injury in osteoarthritis via regulating AMPK/Nrf2 pathway.Journal of molecular histology · 2023Article
- Chondrocyte Homeostasis and Differentiation: Transcriptional Control and Signaling in Healthy and Osteoarthritic Conditions.Life (Basel, Switzerland) · 2023Review
- Osteoarthritis: pathogenic signaling pathways and therapeutic targets.Signal transduction and targeted therapy · 2023Review
- Fibroblast Growth Factors and Cellular Communication Network Factors: Intimate Interplay by the Founding Members in Cartilage.International journal of molecular sciences · 2022Review
- New developments in the biology of fibroblast growth factors.WIREs mechanisms of disease · 2022Review
- CCN proteins in the musculoskeletal system: current understanding and challenges in physiology and pathology.Journal of cell communication and signaling · 2021Review
- Transcriptional profiling of intervertebral disc in a post-traumatic early degeneration organ culture model.JOR spine · 2021Article
- Bipartite regulation of cellular communication network factor 2 and fibroblast growth factor 1 genes by fibroblast growth factor 1 through histone deacetylase 1 and fork head box protein A1.Journal of cell communication and signaling · 2021Article
- Fibroblast growth factor signalling in osteoarthritis and cartilage repair.Nature reviews. Rheumatology · 2020Review
- FGF/FGFR signaling in health and disease.Signal transduction and targeted therapy · 2020Review
- Ablation of low-molecular-weight FGF2 isoform accelerates murine osteoarthritis while loss of high-molecular-weight FGF2 isoforms offers protection.Journal of cellular physiology · 2019Article
- Metabolic regulation of the CCN family genes by glycolysis in chondrocytes.Journal of cell communication and signaling · 2018Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Fibroblast growth factor 1 (FGF-1) is a classical member of the FGF family and is produced by chondrocytes cultured from osteoarthritic patients. Also, this growth factor was shown to bind to CCN family protein 2 (CCN2), which regenerates damaged articular cartilage and counteracts osteoarthritis (OA) in an animal model. However, the pathophysiological role of FGF-1 in cartilage has not been well investigated. In this study, we evaluated the effects of FGF-1 in vitro and its production in vivo by use of an OA model. Treatment of human chondrocytic cells with FGF-1 resulted in marked repression of genes for cartilaginous extracellular matrix components, whereas it strongly induced matrix metalloproteinase 13 (MMP-13), representing its catabolic effects on cartilage. Interestingly, expression of the CCN2 gene was dramatically repressed by FGF-1, which repression eventually caused the reduced production of CCN2 protein from the chondrocytic cells. The results of a reporter gene assay revealed that this repression could be ascribed, at least in part, to transcriptional regulation. In contrast, the gene expression of FGF-1 was enhanced by exogenous FGF-1, indicating a positive feedback system in these cells. Of note, induction of FGF-1 was observed in the articular cartilage of a rat OA model. These results collectively indicate a pathological role of FGF-1 in OA development, which includes an insufficient cartilage regeneration response caused by CCN2 down regulation.
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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.