Evidence map›Paper›PMID 32198215›Full record

ReviewEuropean respiratory review : an official journal of the European Respiratory Society2020

Shared mechanisms of multimorbidity in COPD, atherosclerosis and type-2 diabetes: the neutrophil as a potential inflammatory target.

Michael J Hughes, Helen M McGettrick, Elizabeth Sapey

Registry-linked trialOpen access · diamondAbstract readReview
In one paragraph

Review in European respiratory review : an official journal of the European Respiratory Society, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06308302 (Comparative Effects of Inspiratory Muscle Training vs Expiratory Muscle Training Along With Aerobic Interval Training on Functional Performance and Fatigue Level in COPD Patients), which is not on this map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
4.6field-weighted citation impact, top 4% 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.

NCT06308302 nacompletednot on this mapstarted 2023, after this paper: background citation

Comparative Effects of Inspiratory Muscle Training vs Expiratory Muscle Training Along With Aerobic Interval Training on Functional Performance and Fatigue Level in COPD Patients

TypeinterventionalSponsorRiphah International UniversityRan2023 to 2024Enrolled53ConditionsCOPDArmsGroup A (Inspiratory Muscles Training + Aerobic Interval Training), Group B (Expiratory Muscles Training +Aerobic Interval Training)
3 · Its place in the literature

Who cites it

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.

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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

3 authors at 1 institution in 1 country.

Michael J HughesBirmingham Acute Care Research Group, Institute of Inflammation and Ageing, University of Birmingham, Birmingham, UK mxh619@bham.ac.uk.ORCID https://orcid.org/0000-0002-5793-415X
Helen M McGettrickRheumatology Research Group, Institute of Inflammation and Ageing, University of Birmingham, Birmingham, UK.ORCID https://orcid.org/0000-0002-5950-8840
Elizabeth SapeyBirmingham Acute Care Research Group, Institute of Inflammation and Ageing, University of Birmingham, Birmingham, UK.ORCID https://orcid.org/0000-0003-3454-5482
University of Birmingham · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

Multimorbidity is increasingly common and current healthcare strategies are not always aligned to treat this complex burden of disease. COPD, type-2 diabetes mellitus (T2D) and cardiovascular disease, especially atherosclerosis, occur more frequently together than expected, even when risk factors such as smoking, obesity, inactivity and poverty are considered. This supports the possibility of unifying mechanisms that contribute to the pathogenesis or progression of each condition.Neutrophilic inflammation is causally associated with COPD, and increasingly recognised in the pathogenesis of atherosclerosis and T2D, potentially forming an aetiological link between conditions. This link might reflect an overspill of inflammation from one affected organ into the systemic circulation, exposing all organs to an increased milieu of proinflammatory cytokines. Additionally, increasing evidence supports the involvement of other processes in chronic disease pathogenesis, such as cellular senescence or changes in cellular phenotypes.This review explores the current scientific evidence for inflammation, cellular ageing and cellular processes, such as reactive oxygen species production and phenotypic changes in the pathogenesis of COPD, T2D and atherosclerosis; highlighting common mechanisms shared across these diseases. We identify emerging therapeutic approaches that target these areas, but also where more work is still required to improve our understanding of the underlying cellular biology in a multimorbid disease setting.

Indexed as

AnimalsAtherosclerosisCellular SenescenceDiabetes Mellitus, Type 2HumansImmunosenescenceInflammationInflammation MediatorsMultimorbidityNeutrophilsPulmonary Disease, Chronic ObstructiveRisk AssessmentRisk FactorsSignal TransductionInflammation Mediators

Identifiers

PMID32198215
PMCPMC9488696
OpenAlexW3011783377

What OpenQuestion holds

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LicenceCC BY-NC
Read underepoch 390

Registered trials

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.