ArticleJournal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research2019
Osteocyte Death and Bone Overgrowth in Mice Lacking Fibroblast Growth Factor Receptors 1 and 2 in Mature Osteoblasts and Osteocytes.
Article in Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 35 citations in OpenAlex.
- Fibroblast growth factor receptor signaling in maturing osteoblasts controls cell-matrix interactions critical for osteocyte survival.Bone research · 2026Article
- FGFR1 signaling in rheumatoid arthritis: Mechanisms of bone destruction and therapeutic targeting (Review).International journal of molecular medicine · 2026Review
- Apoptosis of Mdm2-deficient osteocytes enhances osteogenesis through TRPM8-enriched apoptotic vesicles.Bone research · 2026Article
- Fgf18 marks reserve skeletal progenitors in the fibrous periosteum contributing to bone fracture repair.Cell reports · 2026Article
- Fibroblast Growth Factor Receptor Signaling in Maturing Osteoblasts Controls Cell-Matrix Interactions Critical for Osteocyte Survival.bioRxiv : the preprint server for biology · 2026Article
- New knock-in mouse linesJBMR plus · 2026Article
- Endoplasmic reticulum stress disrupts signaling via altered processing of transmembrane receptors.Cell communication and signaling : CCS · 2025Article
- Non-coding RNAs mediate mechanical load-regulating bone metabolic homeostasis.Frontiers in cell and developmental biology · 2025Review
- Metabolic reprogramming in skeletal cell differentiation.Bone research · 2024Review
- Generation of bone-specific lysyl hydroxylase 2 knockout mice and their phenotypes.Biochemistry and biophysics reports · 2024Article
- Review
- Multi-organ phenotypes in mice lacking latent TGFβ binding protein 2 (LTBP2).Developmental dynamics : an official publication of the American Association of Anatomists · 2024Review
- Loss of Fgfr1 and Fgfr2 in Scleraxis-lineage cells leads to enlarged bone eminences and attachment cell death.Developmental dynamics : an official publication of the American Association of Anatomists · 2023Article
- Hypochondroplasia gain-of-function mutation in FGFR3 causes defective bone mineralization in mice.JCI insight · 2023Article
- Wnt/β-Catenin Signaling in Craniomaxillofacial Osteocytes.Current osteoporosis reports · 2023Review
- Overexpression of fibroblast growth factor receptor 2 in bone marrow mesenchymal stem cells enhances osteogenesis and promotes critical cranial bone defect regeneration.Frontiers in cell and developmental biology · 2023Article
- Metformin can mitigate skeletal dysplasia caused by Pck2 deficiency.International journal of oral science · 2022Article
- New developments in the biology of fibroblast growth factors.WIREs mechanisms of disease · 2022Review
- Postnatal Osterix but not DMP1 lineage cells significantly contribute to intramembranous ossification in three preclinical models of bone injury.Frontiers in physiology · 2022Article
- Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Fibroblast growth factor (FGF) signaling pathways have well-established roles in skeletal development, with essential functions in both chondrogenesis and osteogenesis. In mice, previous conditional knockout studies suggested distinct roles for FGF receptor 1 (FGFR1) signaling at different stages of osteogenesis and a role for FGFR2 in osteoblast maturation. However, the potential for redundancy among FGFRs and the mechanisms and consequences of stage-specific osteoblast lineage regulation were not addressed. Here, we conditionally inactivate Fgfr1 and Fgfr2 in mature osteoblasts with an Osteocalcin (OC)-Cre or Dentin matrix protein 1 (Dmp1)-CreER driver. We find that young mice lacking both receptors or only FGFR1 are phenotypically normal. However, between 6 and 12 weeks of age, OC-Cre Fgfr1/Fgfr2 double- and Fgfr1 single-conditional knockout mice develop a high bone mass phenotype with increased periosteal apposition, increased and disorganized endocortical bone with increased porosity, and biomechanical properties that reflect increased bone mass but impaired material properties. Histopathological and gene expression analyses show that this phenotype is preceded by a striking loss of osteocytes and accompanied by activation of the Wnt/β-catenin signaling pathway. These data identify a role for FGFR1 signaling in mature osteoblasts/osteocytes that is directly or indirectly required for osteocyte survival and regulation of bone mass during postnatal bone growth. © 2019 American Society for Bone and Mineral Research.
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Registered trials
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