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Fibroblast growth factor signaling in skeletal development and disease

Fibroblast growth factor (FGF) signaling pathways are essential regulators of vertebrate skeletal development. FGF signaling regulates development of the limb bud and formation of the mesenchymal condensation and has key roles in regulating chondrogenesis, osteogenesis, and bone and mineral homeosta...

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Detalles Bibliográficos
Autores principales: Ornitz, David M., Marie, Pierre J.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Cold Spring Harbor Laboratory Press 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4526732/
https://www.ncbi.nlm.nih.gov/pubmed/26220993
http://dx.doi.org/10.1101/gad.266551.115
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author Ornitz, David M.
Marie, Pierre J.
author_facet Ornitz, David M.
Marie, Pierre J.
author_sort Ornitz, David M.
collection PubMed
description Fibroblast growth factor (FGF) signaling pathways are essential regulators of vertebrate skeletal development. FGF signaling regulates development of the limb bud and formation of the mesenchymal condensation and has key roles in regulating chondrogenesis, osteogenesis, and bone and mineral homeostasis. This review updates our review on FGFs in skeletal development published in Genes & Development in 2002, examines progress made on understanding the functions of the FGF signaling pathway during critical stages of skeletogenesis, and explores the mechanisms by which mutations in FGF signaling molecules cause skeletal malformations in humans. Links between FGF signaling pathways and other interacting pathways that are critical for skeletal development and could be exploited to treat genetic diseases and repair bone are also explored.
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spelling pubmed-45267322016-01-15 Fibroblast growth factor signaling in skeletal development and disease Ornitz, David M. Marie, Pierre J. Genes Dev Review Fibroblast growth factor (FGF) signaling pathways are essential regulators of vertebrate skeletal development. FGF signaling regulates development of the limb bud and formation of the mesenchymal condensation and has key roles in regulating chondrogenesis, osteogenesis, and bone and mineral homeostasis. This review updates our review on FGFs in skeletal development published in Genes & Development in 2002, examines progress made on understanding the functions of the FGF signaling pathway during critical stages of skeletogenesis, and explores the mechanisms by which mutations in FGF signaling molecules cause skeletal malformations in humans. Links between FGF signaling pathways and other interacting pathways that are critical for skeletal development and could be exploited to treat genetic diseases and repair bone are also explored. Cold Spring Harbor Laboratory Press 2015-07-15 /pmc/articles/PMC4526732/ /pubmed/26220993 http://dx.doi.org/10.1101/gad.266551.115 Text en © 2015 Ornitz and Marie; Published by Cold Spring Harbor Laboratory Press http://creativecommons.org/licenses/by-nc/4.0/ This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.
spellingShingle Review
Ornitz, David M.
Marie, Pierre J.
Fibroblast growth factor signaling in skeletal development and disease
title Fibroblast growth factor signaling in skeletal development and disease
title_full Fibroblast growth factor signaling in skeletal development and disease
title_fullStr Fibroblast growth factor signaling in skeletal development and disease
title_full_unstemmed Fibroblast growth factor signaling in skeletal development and disease
title_short Fibroblast growth factor signaling in skeletal development and disease
title_sort fibroblast growth factor signaling in skeletal development and disease
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4526732/
https://www.ncbi.nlm.nih.gov/pubmed/26220993
http://dx.doi.org/10.1101/gad.266551.115
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