4.6 Review

Role of FGF/FGFR signaling in skeletal development and homeostasis: learning from mouse models

Journal

BONE RESEARCH
Volume 2, Issue -, Pages -

Publisher

NATURE PUBLISHING GROUP
DOI: 10.1038/boneres.2014.3

Keywords

-

Funding

  1. National Natural Science Foundation of China [81030036, 81270012, 81170809]
  2. Special Funds for Major State Basic Research Program of China (973 Program) [2014CB942904]
  3. Committee of Science and Technology of Chongqing [CSTC 2011jjA1468]
  4. national key laboratory [SKLZZ201017]

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Fibroblast growth factor (FGF)/fibroblast growth factor receptor (FGFR) signaling plays essential roles in bone development and diseases. Missense mutations in FGFs and FGFRs in humans can cause various congenital bone diseases, including chondrodysplasia syndromes, craniosynostosis syndromes and syndromes with dysregulated phosphate metabolism. FGF/FGFR signaling is also an important pathway involved in the maintenance of adult bone homeostasis. Multiple kinds of mouse models, mimicking human skeleton diseases caused by missense mutations in FGFs and FGFRs, have been established by knock-in/out and transgenic technologies. These genetically modified mice provide good models for studying the role of FGF/FGFR signaling in skeleton development and homeostasis. In this review, we summarize the mouse models of FGF signaling-related skeleton diseases and recent progresses regarding the molecular mechanisms, underlying the role of FGFs/FGFRs in the regulation of bone development and homeostasis. This review also provides a perspective view on future works to explore the roles of FGF signaling in skeletal development and homeostasis.

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