Evidence map›Paper›PMID 42682829›Full record

ArticleERJ open research2026

Proteome-wide Mendelian randomisation of lung function to identify potential therapeutic targets for respiratory disease.

Jing Chen, Nick Shrine, Kayesha Coley, Richard J Packer, Ahmed Edris, Abril G Izquierdo, Brandon Lim, Mikyeong Lee, Frank Dudbridge, Robin G Walters and 5 more

Abstract read
In one paragraph

Article in ERJ open research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

15 authors.

Jing ChenDivision of Public Health and Epidemiology, School of Medical Sciences, University of Leicester, Leicester, UK.ORCID https://orcid.org/0000-0003-1287-1930
Nick ShrineDivision of Public Health and Epidemiology, School of Medical Sciences, University of Leicester, Leicester, UK.ORCID https://orcid.org/0000-0003-3641-4371
Kayesha ColeyDivision of Public Health and Epidemiology, School of Medical Sciences, University of Leicester, Leicester, UK.ORCID https://orcid.org/0000-0003-4951-6799
Richard J PackerDivision of Public Health and Epidemiology, School of Medical Sciences, University of Leicester, Leicester, UK.ORCID https://orcid.org/0000-0003-2459-1020
Ahmed EdrisNuffield Department of Population Health, University of Oxford, Oxford, UK.
Abril G IzquierdoDivision of Public Health and Epidemiology, School of Medical Sciences, University of Leicester, Leicester, UK.
Brandon LimDivision of Public Health and Epidemiology, School of Medical Sciences, University of Leicester, Leicester, UK.
Mikyeong LeeEpidemiology Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC, USA.ORCID https://orcid.org/0000-0002-3036-3684
Frank DudbridgeDivision of Public Health and Epidemiology, School of Medical Sciences, University of Leicester, Leicester, UK.
Robin G WaltersNuffield Department of Population Health, University of Oxford, Oxford, UK.
Ian P HallDivision of Respiratory Medicine and NIHR Nottingham Biomedical Research Centre, University of Nottingham, Nottingham, UK.
Louise V WainDivision of Public Health and Epidemiology, School of Medical Sciences, University of Leicester, Leicester, UK.ORCID https://orcid.org/0000-0003-4951-1867
Martin D TobinDivision of Public Health and Epidemiology, School of Medical Sciences, University of Leicester, Leicester, UK.
Anna L GuyattDivision of Public Health and Epidemiology, School of Medical Sciences, University of Leicester, Leicester, UK.ORCID https://orcid.org/0000-0003-1860-6337
SpiroMeta Consortium and the CHARGE consortium

Funding

Wellcome Trust
6 · The paper itself

Abstract

Background: Despite multiple clinical trials, disease-modifying treatments for COPD are currently limited. Since many drugs target proteins, identifying causality between proteins and lung function informs understanding of COPD pathophysiology and may suggest novel targets. We used Mendelian randomisation (MR) to prioritise proteins as potentially causal for imparied lung function. For prioritised proteins, we explored their potential suitability as drug targets by predicting their effects on a range of clinical outcomes. Methods: We used genome-wide association study (GWAS) data on 2923 proteins (n=48 195, UK Biobank) to identify single genetic variants (protein quantitative trait loci (cis-pQTLs)) associated with protein levels (p≤5×10 Findings: 1841 proteins had a suitable cis-pQTL. We implicated 16 proteins as potentially causal for lung function (p<1.71×10 Interpretation: Our approach identifies proteins (some novel) that are potentially therapeutic targets for respiratory disease, and which warrant follow-up for utility and safety.

Identifiers

PMID42682829
PMCPMC13531259

What OpenQuestion holds

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Registered trials

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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.