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Notch signaling in lung diseases: focus on Notch1 and Notch3

Notch signaling is an evolutionarily conserved cell–cell communication mechanism that plays a key role in lung homeostasis, injury and repair. The loss of regulation of Notch signaling, especially Notch1 and Notch3, has recently been linked to the pathogenesis of important lung diseases, in particul...

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Detalles Bibliográficos
Autores principales: Zong, Dandan, Ouyang, Ruoyun, Li, Jinhua, Chen, Yan, Chen, Ping
Formato: Online Artículo Texto
Lenguaje:English
Publicado: SAGE Publications 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5933616/
https://www.ncbi.nlm.nih.gov/pubmed/27378579
http://dx.doi.org/10.1177/1753465816654873
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author Zong, Dandan
Ouyang, Ruoyun
Li, Jinhua
Chen, Yan
Chen, Ping
author_facet Zong, Dandan
Ouyang, Ruoyun
Li, Jinhua
Chen, Yan
Chen, Ping
author_sort Zong, Dandan
collection PubMed
description Notch signaling is an evolutionarily conserved cell–cell communication mechanism that plays a key role in lung homeostasis, injury and repair. The loss of regulation of Notch signaling, especially Notch1 and Notch3, has recently been linked to the pathogenesis of important lung diseases, in particular, chronic obstructive pulmonary disease (COPD), asthma, pulmonary fibrosis, pulmonary arterial hypertension (PAH), lung cancer and lung lesions in some congenital diseases. This review focuses on recent advances related to the mechanisms and the consequences of aberrant or absent Notch1/3 activity in the initiation and progression of lung diseases. Our increasing understanding of this signaling pathway offers great hope that manipulating Notch signaling may represent a promising alternative complementary therapeutic strategy in the future.
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spelling pubmed-59336162018-05-09 Notch signaling in lung diseases: focus on Notch1 and Notch3 Zong, Dandan Ouyang, Ruoyun Li, Jinhua Chen, Yan Chen, Ping Ther Adv Respir Dis Reviews Notch signaling is an evolutionarily conserved cell–cell communication mechanism that plays a key role in lung homeostasis, injury and repair. The loss of regulation of Notch signaling, especially Notch1 and Notch3, has recently been linked to the pathogenesis of important lung diseases, in particular, chronic obstructive pulmonary disease (COPD), asthma, pulmonary fibrosis, pulmonary arterial hypertension (PAH), lung cancer and lung lesions in some congenital diseases. This review focuses on recent advances related to the mechanisms and the consequences of aberrant or absent Notch1/3 activity in the initiation and progression of lung diseases. Our increasing understanding of this signaling pathway offers great hope that manipulating Notch signaling may represent a promising alternative complementary therapeutic strategy in the future. SAGE Publications 2016-07-04 2016-10 /pmc/articles/PMC5933616/ /pubmed/27378579 http://dx.doi.org/10.1177/1753465816654873 Text en © The Author(s), 2016 http://creativecommons.org/licenses/by-nc/3.0/ This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 3.0 License (http://www.creativecommons.org/licenses/by-nc/3.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page (https://us.sagepub.com/en-us/nam/open-access-at-sage).
spellingShingle Reviews
Zong, Dandan
Ouyang, Ruoyun
Li, Jinhua
Chen, Yan
Chen, Ping
Notch signaling in lung diseases: focus on Notch1 and Notch3
title Notch signaling in lung diseases: focus on Notch1 and Notch3
title_full Notch signaling in lung diseases: focus on Notch1 and Notch3
title_fullStr Notch signaling in lung diseases: focus on Notch1 and Notch3
title_full_unstemmed Notch signaling in lung diseases: focus on Notch1 and Notch3
title_short Notch signaling in lung diseases: focus on Notch1 and Notch3
title_sort notch signaling in lung diseases: focus on notch1 and notch3
topic Reviews
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5933616/
https://www.ncbi.nlm.nih.gov/pubmed/27378579
http://dx.doi.org/10.1177/1753465816654873
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