The pathogenesis of asthma is complex and multi-faceted. Asthma patients have a diverse range of underlying dominant disease processes and pathways despite apparent similarities in clinical expression. Here, we present the current understanding of asthma pathogenesis. We discuss airway inflammation (both T2HIGH and T2LOW), airway hyperresponsiveness (AHR) and airways remodelling as four key factors in asthma pathogenesis, and also outline other contributory factors such as genetics and co-morbidities. Response to current asthma therapies also varies greatly, which is probably related to the inter-patient differences in pathogenesis. Here, we also summarize how our developing understanding of detailed pathological processes potentially translates into the targeted treatment options we require for optimal asthma management in the future.
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July 2017
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This issue of Clinical Science showcases review articles covering kidney disease, the respiratory system, neurology and oxidative stress.
Review Article|
June 30 2017
Pathogenesis of asthma: implications for precision medicine
Richard J. Russell;
Richard J. Russell
1Department of Infection, Immunity and Inflammation, Institute for Lung Health, Glenfield Hospital, University of Leicester, LE3 9QP, U.K.
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Christopher Brightling
1Department of Infection, Immunity and Inflammation, Institute for Lung Health, Glenfield Hospital, University of Leicester, LE3 9QP, U.K.
Correspondence: C.E. Brightling ([email protected])
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Publisher: Portland Press Ltd
Received:
March 15 2017
Revision Received:
May 02 2017
Accepted:
May 08 2017
Online ISSN: 1470-8736
Print ISSN: 0143-5221
© 2017 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society
2017
Clin Sci (Lond) (2017) 131 (14): 1723–1735.
Article history
Received:
March 15 2017
Revision Received:
May 02 2017
Accepted:
May 08 2017
Citation
Richard J. Russell, Christopher Brightling; Pathogenesis of asthma: implications for precision medicine. Clin Sci (Lond) 15 July 2017; 131 (14): 1723–1735. doi: https://doi.org/10.1042/CS20160253
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