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Factors controlling airway smooth muscle proliferation in asthma

Factors controlling airway smooth muscle proliferation in asthma Airway smooth muscle proliferation has been the focus of considerable attention, as it is a quantitatively important component of the airway wall remodeling response in asthma and has been suggested as a suitable target for the development of novel anti-asthma agents. Such agents are considered likely to reduce airway hyperresponsiveness and, consequently, airway obstruction, resulting in fewer symptoms and exacerbations. Identifying suitable drug targets has proved an elusive goal, as no dominant molecular mechanism for remodeling has emerged. Moreover, recent findings raise some doubt as to whether smooth muscle proliferation per se is the explanation of the increase in smooth muscle cell number in asthma, with alternative explanations including the proposal that cells migrate either from the interstitial compartment or from a circulating precursor stem cell population. Therefore, drug targeting of migration responses should be considered as an alternative approach to regulating the smooth muscle component of airway wall remodeling. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Current Allergy and Asthma Reports Springer Journals

Factors controlling airway smooth muscle proliferation in asthma

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References (63)

Publisher
Springer Journals
Copyright
Copyright © 2004 by Current Science Inc
Subject
Medicine & Public Health; Allergology; Pneumology/Respiratory System; Otorhinolaryngology; Infectious Diseases
ISSN
1529-7322
eISSN
1534-6315
DOI
10.1007/s11882-004-0055-8
Publisher site
See Article on Publisher Site

Abstract

Airway smooth muscle proliferation has been the focus of considerable attention, as it is a quantitatively important component of the airway wall remodeling response in asthma and has been suggested as a suitable target for the development of novel anti-asthma agents. Such agents are considered likely to reduce airway hyperresponsiveness and, consequently, airway obstruction, resulting in fewer symptoms and exacerbations. Identifying suitable drug targets has proved an elusive goal, as no dominant molecular mechanism for remodeling has emerged. Moreover, recent findings raise some doubt as to whether smooth muscle proliferation per se is the explanation of the increase in smooth muscle cell number in asthma, with alternative explanations including the proposal that cells migrate either from the interstitial compartment or from a circulating precursor stem cell population. Therefore, drug targeting of migration responses should be considered as an alternative approach to regulating the smooth muscle component of airway wall remodeling.

Journal

Current Allergy and Asthma Reports – Springer Journals

Published: May 27, 2004

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