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Fully integrating pathophysiological insights in copd: An updated working disease model to broaden therapeutic vision

Walters, EH, Shukla, SD, Mahmood, Malik Quasir and Ward, C 2021, Fully integrating pathophysiological insights in copd: An updated working disease model to broaden therapeutic vision, European Respiratory Review, vol. 30, no. 160, pp. 1-15, doi: 10.1183/16000617.0364-2020.

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Title Fully integrating pathophysiological insights in copd: An updated working disease model to broaden therapeutic vision
Author(s) Walters, EH
Shukla, SD
Mahmood, Malik Quasir
Ward, C
Journal name European Respiratory Review
Volume number 30
Issue number 160
Article ID 200364
Start page 1
End page 15
Total pages 15
Publisher European Respiratory Society
Place of publication Copenhagen, Denmark
Publication date 2021
ISSN 0905-9180
1600-0617
Keyword(s) CELLS
EPITHELIAL-MESENCHYMAL TRANSITION
FEV1 DECLINE
GLOBAL STRATEGY
HUMAN LUNG
INFLAMMATION
Life Sciences & Biomedicine
OBSTRUCTIVE PULMONARY-DISEASE
RECEPTOR
Respiratory System
Science & Technology
SMALL-AIRWAY-OBSTRUCTION
SMOKERS
Summary Our starting point is that relatively new findings into the pathogenesis and pathophysiology of airway disease in smokers that lead to chronic obstructive pulmonary disease (COPD) need to be reassessed as a whole and integrated into “mainstream” thinking along with traditional concepts which have stood the test of time. Such a refining of the accepted disease paradigm is urgently needed as thinking on therapeutic targets is currently under active reconsideration. We feel that generalised airway wall “inflammation” is unduly over-emphasised, and highlight the patchy and variable nature of the pathology (with the core being airway remodelling). In addition, we present evidence for airway wall disease in smokers/COPD as including a hypocellular, hypovascular, destructive, fibrotic pathology, with a likely spectrum of epithelial–mesenchymal transition states as significant drivers of this remodelling. Furthermore, we present data from a number of research modalities and integrate this with the aetiology of lung cancer, the role of chronic airway luminal colonisation/infection by a specific group of “respiratory” bacteria in smokers (which results in luminal inflammation) and the central role for oxidative stress on the epithelium. We suggest translation of these insights into more focus on asymptomatic smokers and early COPD, with the potential for fresh preventive and therapeutic approaches.
Language eng
DOI 10.1183/16000617.0364-2020
Field of Research 1116 Medical Physiology
HERDC Research category C1 Refereed article in a scholarly journal
Free to Read? Yes
Persistent URL http://hdl.handle.net/10536/DRO/DU:30152311

Document type: Journal Article
Collections: Faculty of Health
School of Medicine
Open Access Collection
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Every reasonable effort has been made to ensure that permission has been obtained for items included in DRO. If you believe that your rights have been infringed by this repository, please contact drosupport@deakin.edu.au.