Fibroblast growth factor signaling controlling bone formation: An update

被引:65
作者
Marie, Pierre J. [1 ,2 ]
机构
[1] INSERM, U606, Lab Osteoblast Biol & Pathol, F-75475 Paris 10, France
[2] Univ Paris Diderot, Lariboisiere Hosp, F-75475 Paris 10, France
关键词
FGF; Signaling; Osteoblast; Bone formation; FACTOR RECEPTOR-2 FGFR2; MESENCHYMAL STEM-CELLS; OSTEOBLAST DIFFERENTIATION; CALVARIAL BONE; APERT-SYNDROME; MORPHOGENETIC PROTEIN-2; MOUSE MODEL; CRANIOSYNOSTOSIS; MUTATION; ACTIVATION;
D O I
10.1016/j.gene.2012.01.086
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Fibroblast Growth Factors (FGFs) regulate prenatal and postnatal bone formation through activation of FGF receptors (FGFR) and downstream signaling events. During the last decade, major advances have been made in our understanding of the mechanisms by which FGF/FGFR signaling controls osteoprogenitor cell replication and osteoblast differentiation and function. The analysis of the phenotype induced by FGF invalidation and mutations in FGFR allowed to delineate key FGF signaling pathways that regulate osteoblastogenesis. Molecular genomic studies led to identify target genes that are controlled by FGF/FGFR signaling and govern osteoblasts. The analysis of intracellular signaling pathways showed the importance of functional crosstalks between FGF signaling and other pathways in the regulation of bone formation. These recent progresses in the mechanisms underlying FGF/FGFR signaling may provide a molecular basis for developing therapeutic strategies in human skeletal dysplasias. (C) 2012 Elsevier B.V. All rights reserved.
引用
收藏
页码:1 / 4
页数:4
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