ArticleEndocrinology2018
FGF23 Regulates Wnt/β-Catenin Signaling-Mediated Osteoarthritis in Mice Overexpressing High-Molecular-Weight FGF2.
Article in Endocrinology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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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Who cites it
29 citing papers in PubMed, 43 citations in OpenAlex.
- The hsa_circ_0084050/miR-373-3p Axis Controls Bone Sialoprotein-Induced ADAM9 Upregulation to Drive Lung Cancer Progression and Metastasis.International journal of molecular sciences · 2026Article
- Osteoarthritis as a systemic disorder: multi-organ crosstalk in pathogenesis and therapeutic targeting.Frontiers in immunology · 2026Review
- Intertwined roles of microRNA-155 and metformin in osteoarthritis: Novel potential diagnostic, prognostic, and therapeutic modulators.World journal of orthopedics · 2025Review
- FGF8 promotes lipid droplet accumulation via the FGFR1/p-p38 axis in chondrocytes.Acta biochimica et biophysica Sinica · 2025Article
- Association of organs-crosstalk with the pathogenesis of osteoarthritis: cartilage as a key player.Frontiers in endocrinology · 2025Review
- Role of signaling pathways in age-related orthopedic diseases: focus on the fibroblast growth factor family.Military Medical Research · 2024Review
- Signalling interaction between β-catenin and other signalling molecules during osteoarthritis development.Cell proliferation · 2024Review
- Article
- The direct effect of fibroblast growth factor 23 on vascular smooth muscle cell phenotype and function.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2023Article
- Anticipated effects of burosumab treatment on long-term clinical sequelae in XLH: expert perspectives.Frontiers in endocrinology · 2023Article
- FGF receptor inhibitor BGJ398 partially rescues osteoarthritis-like phenotype in older high molecular weight FGF2 transgenic mice via multiple mechanisms.Scientific reports · 2022Article
- Cellular and Molecular Alterations Underlying Abnormal Bone Growth in X-Linked Hypophosphatemia.International journal of molecular sciences · 2022Review
- An Expert Perspective on Phosphate Dysregulation With a Focus on Chronic Hypophosphatemia.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2022Article
- Roles of the fibroblast growth factor signal transduction system in tissue injury repair.Burns & trauma · 2022Review
- The Wnt signaling cascade in the pathogenesis of osteoarthritis and related promising treatment strategies.Frontiers in physiology · 2022Review
- Bioinformatics-Based Research on Key Genes and Pathways of Intervertebral Disc Degeneration.Cartilage · 2021Article
- Gait disturbances and muscle dysfunction in fibroblast growth factor 2 knockout mice.Scientific reports · 2021Article
- Omega-3 fatty acid modulation of serum and osteocyte tumor necrosis factor-α in adult mice exposed to ionizing radiation.Journal of applied physiology (Bethesda, Md. : 1985) · 2021Article
- What Can We Learn from FGF-2 Isoform-Specific Mouse Mutants? Differential Insights into FGF-2 Physiology In Vivo.International journal of molecular sciences · 2020Review
- Fibroblast growth factor signalling in osteoarthritis and cartilage repair.Nature reviews. Rheumatology · 2020Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Although humans with X-linked hypophosphatemia (XLH) and the Hyp mouse, a murine homolog of XLH, are known to develop degenerative joint disease, the exact mechanism that drives the osteoarthritis (OA) phenotype remains unclear. Mice that overexpress high-molecular-weight fibroblast growth factor (FGF) 2 isoforms (HMWTg mice) phenocopy both XLH and Hyp, including OA with increased FGF23 production in bone and serum. Because HMWTg cartilage also has increased FGF23 and there is cross-talk between FGF23-Wnt/β-catenin signaling, the purpose of this study was to determine if OA observed in HMWTg mice is due to FGF23-mediated canonical Wnt signaling in chondrocytes, given that both pathways are implicated in OA pathogenesis. HMWTg OA joints had decreased Dkk1, Sost, and Lrp6 expression with increased Wnt5a, Wnt7b, Lrp5, Axin2, phospho-GSK3β, Lef1, and nuclear β-catenin, as indicated by immunohistochemistry or quantitative PCR analysis. Chondrocytes from HMWTg mice had enhanced alcian blue and alkaline phosphatase staining as well as increased FGF23, Adamts5, Il-1β, Wnt7b, Wnt16, and Wisp1 gene expression and phospho-GSK3β protein expression as indicated by Western blot, compared with chondrocytes of vector control and chondrocytes from mice overexpressing the low-molecular-weight isoform, which were protected from OA. Canonical Wnt inhibitor treatment rescued some of those parameters in HMWTg chondrocytes, seemingly delaying the initially accelerated chondrogenic differentiation. FGF23 neutralizing antibody treatment was able to partly ameliorate OA abnormalities in subchondral bone and reduce degradative/hypertrophic chondrogenic marker expression in HMWTg joints in vivo. These results demonstrate that osteoarthropathy of HMWTg is at least partially due to FGF23-modulated Wnt/β-catenin signaling in chondrocytes.
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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.