FGF signaling pathways in endochondral and intramembranous bone development and human genetic disease

FGF signaling pathways in endochondral and intramembranous bone development and human genetic disease

2002 | David M. Ornitz and Pierre J. Marie
This article discusses the critical role of FGF signaling pathways in both endochondral and intramembranous bone development, as well as their involvement in human genetic diseases. FGF signaling is essential for early limb development and throughout skeletal development. The review explores how FGF signaling interacts with other major signaling pathways that regulate chondrogenesis and osteogenesis. Endochondral ossification forms long bones and involves a cartilaginous template, while intramembranous ossification forms flat bones directly without a cartilage intermediate. Mutations in FGF receptors are linked to various skeletal disorders, such as achondroplasia, thanatophoric dysplasia, and craniosynostosis syndromes. These mutations often result in gain-of-function effects, leading to abnormal skeletal development. The article also details the molecular mechanisms of FGF signaling, including the roles of FGF receptors, ligands, and interactions with other signaling molecules like IHH, PTHrP, and BMPs. The importance of FGF signaling in regulating chondrocyte proliferation, differentiation, and apoptosis is emphasized, as well as its role in intramembranous bone formation and cranial suture development. The article highlights the complexity of FGF signaling in skeletal development and its implications for understanding and treating skeletal disorders.This article discusses the critical role of FGF signaling pathways in both endochondral and intramembranous bone development, as well as their involvement in human genetic diseases. FGF signaling is essential for early limb development and throughout skeletal development. The review explores how FGF signaling interacts with other major signaling pathways that regulate chondrogenesis and osteogenesis. Endochondral ossification forms long bones and involves a cartilaginous template, while intramembranous ossification forms flat bones directly without a cartilage intermediate. Mutations in FGF receptors are linked to various skeletal disorders, such as achondroplasia, thanatophoric dysplasia, and craniosynostosis syndromes. These mutations often result in gain-of-function effects, leading to abnormal skeletal development. The article also details the molecular mechanisms of FGF signaling, including the roles of FGF receptors, ligands, and interactions with other signaling molecules like IHH, PTHrP, and BMPs. The importance of FGF signaling in regulating chondrocyte proliferation, differentiation, and apoptosis is emphasized, as well as its role in intramembranous bone formation and cranial suture development. The article highlights the complexity of FGF signaling in skeletal development and its implications for understanding and treating skeletal disorders.
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