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Origins of increased airway smooth muscle mass in asthma

Asthma is characterized by both chronic inflammation and airway remodeling. Remodeling - the structural changes seen in asthmatic airways - is pivotal in the pathogenesis of the disease. Although significant advances have been made recently in understanding the different aspects of airway remodeling...

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Detalles Bibliográficos
Autores principales: Berair, Rachid, Saunders, Ruth, Brightling, Christopher E
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3688527/
https://www.ncbi.nlm.nih.gov/pubmed/23742314
http://dx.doi.org/10.1186/1741-7015-11-145
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author Berair, Rachid
Saunders, Ruth
Brightling, Christopher E
author_facet Berair, Rachid
Saunders, Ruth
Brightling, Christopher E
author_sort Berair, Rachid
collection PubMed
description Asthma is characterized by both chronic inflammation and airway remodeling. Remodeling - the structural changes seen in asthmatic airways - is pivotal in the pathogenesis of the disease. Although significant advances have been made recently in understanding the different aspects of airway remodeling, the exact biology governing these changes remains poorly understood. There is broad agreement that, in asthma, increased airway smooth muscle mass, in part due to smooth muscle hyperplasia, is a very significant component of airway remodeling. However, significant debate persists on the origins of these airway smooth muscle cells. In this review article we will explore the natural history of airway remodeling in asthma and we will discuss the possible contribution of progenitors, stem cells and epithelial cells in mesenchymal cell changes, namely airway smooth muscle hyperplasia seen in the asthmatic airways.
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spelling pubmed-36885272013-06-25 Origins of increased airway smooth muscle mass in asthma Berair, Rachid Saunders, Ruth Brightling, Christopher E BMC Med Minireview Asthma is characterized by both chronic inflammation and airway remodeling. Remodeling - the structural changes seen in asthmatic airways - is pivotal in the pathogenesis of the disease. Although significant advances have been made recently in understanding the different aspects of airway remodeling, the exact biology governing these changes remains poorly understood. There is broad agreement that, in asthma, increased airway smooth muscle mass, in part due to smooth muscle hyperplasia, is a very significant component of airway remodeling. However, significant debate persists on the origins of these airway smooth muscle cells. In this review article we will explore the natural history of airway remodeling in asthma and we will discuss the possible contribution of progenitors, stem cells and epithelial cells in mesenchymal cell changes, namely airway smooth muscle hyperplasia seen in the asthmatic airways. BioMed Central 2013-06-06 /pmc/articles/PMC3688527/ /pubmed/23742314 http://dx.doi.org/10.1186/1741-7015-11-145 Text en Copyright © 2013 Berair et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Minireview
Berair, Rachid
Saunders, Ruth
Brightling, Christopher E
Origins of increased airway smooth muscle mass in asthma
title Origins of increased airway smooth muscle mass in asthma
title_full Origins of increased airway smooth muscle mass in asthma
title_fullStr Origins of increased airway smooth muscle mass in asthma
title_full_unstemmed Origins of increased airway smooth muscle mass in asthma
title_short Origins of increased airway smooth muscle mass in asthma
title_sort origins of increased airway smooth muscle mass in asthma
topic Minireview
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3688527/
https://www.ncbi.nlm.nih.gov/pubmed/23742314
http://dx.doi.org/10.1186/1741-7015-11-145
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