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FGF Signaling in Lung Development and Disease: Human Versus Mouse
Fibroblast growth factor 10 (FGF10) plays an important role in mouse lung development, injury, and repair. It is considered the main morphogen driving lung branching morphogenesis in rodents. While many studies have found FGF10 SNPs associated with COPD and branch variants in COPD smokers, there is...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6423913/ https://www.ncbi.nlm.nih.gov/pubmed/30930931 http://dx.doi.org/10.3389/fgene.2019.00170 |
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author | Danopoulos, Soula Shiosaki, Jessica Al Alam, Denise |
author_facet | Danopoulos, Soula Shiosaki, Jessica Al Alam, Denise |
author_sort | Danopoulos, Soula |
collection | PubMed |
description | Fibroblast growth factor 10 (FGF10) plays an important role in mouse lung development, injury, and repair. It is considered the main morphogen driving lung branching morphogenesis in rodents. While many studies have found FGF10 SNPs associated with COPD and branch variants in COPD smokers, there is no evidence of a causative role for FGF10 or these SNPs in human lung development and pediatric lung diseases. We and others have shown divergent roles for FGF10 in mouse lung development and early human lung development. Herein, we only review the existing literature on FGF signaling in human lung development and pediatric human lung diseases, comparing what is known in mouse lung to that in human lung. |
format | Online Article Text |
id | pubmed-6423913 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-64239132019-03-29 FGF Signaling in Lung Development and Disease: Human Versus Mouse Danopoulos, Soula Shiosaki, Jessica Al Alam, Denise Front Genet Genetics Fibroblast growth factor 10 (FGF10) plays an important role in mouse lung development, injury, and repair. It is considered the main morphogen driving lung branching morphogenesis in rodents. While many studies have found FGF10 SNPs associated with COPD and branch variants in COPD smokers, there is no evidence of a causative role for FGF10 or these SNPs in human lung development and pediatric lung diseases. We and others have shown divergent roles for FGF10 in mouse lung development and early human lung development. Herein, we only review the existing literature on FGF signaling in human lung development and pediatric human lung diseases, comparing what is known in mouse lung to that in human lung. Frontiers Media S.A. 2019-03-12 /pmc/articles/PMC6423913/ /pubmed/30930931 http://dx.doi.org/10.3389/fgene.2019.00170 Text en Copyright © 2019 Danopoulos, Shiosaki and Al Alam. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Genetics Danopoulos, Soula Shiosaki, Jessica Al Alam, Denise FGF Signaling in Lung Development and Disease: Human Versus Mouse |
title | FGF Signaling in Lung Development and Disease: Human Versus Mouse |
title_full | FGF Signaling in Lung Development and Disease: Human Versus Mouse |
title_fullStr | FGF Signaling in Lung Development and Disease: Human Versus Mouse |
title_full_unstemmed | FGF Signaling in Lung Development and Disease: Human Versus Mouse |
title_short | FGF Signaling in Lung Development and Disease: Human Versus Mouse |
title_sort | fgf signaling in lung development and disease: human versus mouse |
topic | Genetics |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6423913/ https://www.ncbi.nlm.nih.gov/pubmed/30930931 http://dx.doi.org/10.3389/fgene.2019.00170 |
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