Evidence map›Paper›PMID 34039673›Full record

ReviewEuropean respiratory review : an official journal of the European Respiratory Society2021

Fully integrating pathophysiological insights in COPD: an updated working disease model to broaden therapeutic vision.

E Haydn Walters, Shakti D Shukla, Malik Q Mahmood, Chris Ward

Open access · diamondAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in European respiratory review : an official journal of the European Respiratory Society, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 2 pooled it
2.5field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 2 syntheses or guidelines pooled it, 26 citations in OpenAlex.

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  16. Air Pollution as a Risk Factor for Lung Cancer: Potential Mechanisms.American journal of respiratory and critical care medicine · 2022
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 4 institutions in 2 countries.

E Haydn WaltersSchool of Medicine and Menzies Institute, University of Tasmania, Hobart, Australia Haydn.Walters@utas.edu.au.
Shakti D ShuklaPriority Research Centre for Healthy Lungs and School of Medicine and Public Health, Faculty of Health and Medicine, University of Newcastle, Callaghan, Australia.ORCID https://orcid.org/0000-0002-5796-0171
Malik Q MahmoodSchool of Medicine, Faculty of Health, Deakin University, Waurn Ponds, Australia.
Chris WardTranslational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University Medical School, Newcastle University, UK.
Deakin University · AUHunter Medical Research Institute · AUNewcastle University · GBUniversity of Tasmania · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

Pulmonary Disease, Chronic ObstructiveAirway RemodelingHumansInflammationOxidative StressRespiratory System

Identifiers

PMID34039673
PMCPMC9488955
OpenAlexW3164339287

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.