期刊
JOURNAL OF MOLECULAR ENDOCRINOLOGY
卷 53, 期 1, 页码 T11-T34出版社
BIOSCIENTIFICA LTD
DOI: 10.1530/JME-14-0012
关键词
FGF signaling; growth plate; disorder; mouse model; review
资金
- Special Funds from Major State Basic Research Program of China (973 program) [2014CB942904]
- National Natural Science Foundation of China [81220108020, 81030036, 81170809, 81301593]
Skeletons are formed through two distinct developmental actions, intramembranous ossification and endochondral ossification. During embryonic development, most bone is formed by endochondral ossification. The growth plate is the developmental center for endochondral ossification. Multiple signaling pathways participate in the regulation of endochondral ossification. Fibroblast growth factor (FGF)/FGF receptor (FGFR) signaling has been found to play a vital role in the development and maintenance of growth plates. Missense mutations in FGFs and FGFRs can cause multiple genetic skeletal diseases with disordered endochondral ossification. Clarifying the molecular mechanisms of FGFs/FGFRs signaling in skeletal development and genetic skeletal diseases will have implications for the development of therapies for FGF-signaling-related skeletal dysplasias and growth plate injuries. In this review, we summarize the recent advances in elucidating the role of FGFs/FGFRs signaling in growth plate development, genetic skeletal disorders, and the promising therapies for those genetic skeletal diseases resulting from FGFs/FGFRs dysfunction. Finally, we also examine the potential important research in this field in the future.
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