Evidence map›Paper›PMID 40675770›Full record

ArticleThe European respiratory journal2025

Genomics of chronic dry cough unravels neurological pathways.

Kayesha Coley, Catherine John, Jonas Ghouse, David J Shepherd, Nick Shrine, Abril G Izquierdo, Stavroula Kanoni, Emma F Magavern, Richard Packer, Lorcan McGarvey and 14 more

Abstract read
In one paragraph

Article in The European respiratory journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Vine Tea (International journal of molecular sciences · 2026
    Article
  5. Article
  6. Review
  7. Article
  8. Dissecting the genetics of chronic cough.The European respiratory journal · 2025
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

24 authors.

Kayesha ColeyDepartment of Population Health Sciences, University of Leicester, Leicester, UK kayesha.coley@leicester.ac.uk.ORCID https://orcid.org/0000-0003-4951-6799
Catherine JohnDepartment of Population Health Sciences, University of Leicester, Leicester, UK.ORCID https://orcid.org/0000-0002-6057-2073
Jonas GhouseLaboratory for Molecular Cardiology, Department of Cardiology, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark.ORCID https://orcid.org/0000-0002-9634-5964
David J ShepherdDepartment of Population Health Sciences, University of Leicester, Leicester, UK.
Nick ShrineDepartment of Population Health Sciences, University of Leicester, Leicester, UK.ORCID https://orcid.org/0000-0003-3641-4371
Abril G IzquierdoDepartment of Population Health Sciences, University of Leicester, Leicester, UK.
Stavroula KanoniWilliam Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, UK.ORCID https://orcid.org/0000-0002-1691-9615
Emma F MagavernWilliam Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, UK.ORCID https://orcid.org/0000-0003-0699-6411
Richard PackerDepartment of Population Health Sciences, University of Leicester, Leicester, UK.ORCID https://orcid.org/0000-0003-2459-1020
Lorcan McGarveyWellcome-Wolfson Institute for Experimental Medicine, School of Medicine, Dentistry and Biomedical Sciences, Queen's University Belfast, Belfast, UK.ORCID https://orcid.org/0000-0002-2860-0302
Jaclyn A SmithDivision of Immunology, Immunity to Infection and Respiratory Medicine, The University of Manchester, Manchester University NHS Foundation Trust, Manchester, UK.ORCID https://orcid.org/0000-0001-8837-4928
Henning BundgaardDepartment of Cardiology, Copenhagen University Hospital, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.ORCID https://orcid.org/0000-0002-0563-7049
Sisse R OstrowskiDepartment of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark.ORCID https://orcid.org/0000-0001-5288-3851
Christian ErikstrupDepartment of Clinical Immunology, Aarhus University Hospital, Aarhus, Denmark.
Ole B V PedersenDepartment of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark.
David A van HeelBlizard Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, UK.ORCID https://orcid.org/0000-0002-0637-2265
Genes and Health Research Team
William HennahOrion Pharma, Espoo, Finland.ORCID https://orcid.org/0000-0002-4462-4208
Mikko MarttilaOrion Pharma, Nottingham, UK.
Robert C FreeUniversity Hospitals of Leicester NHS Trust, Leicester, UK.ORCID https://orcid.org/0000-0001-8053-435X
Edward J HolloxDepartment of Genetics and Genome Biology, University of Leicester, Leicester, UK.ORCID https://orcid.org/0000-0002-0115-2298
Louise V WainDepartment of Population Health Sciences, University of Leicester, Leicester, UK.ORCID https://orcid.org/0000-0003-4951-1867
Martin D TobinDepartment of Population Health Sciences, University of Leicester, Leicester, UK.ORCID https://orcid.org/0000-0002-3596-7874
Chiara BatiniDepartment of Population Health Sciences, University of Leicester, Leicester, UK.ORCID https://orcid.org/0000-0002-7140-2985

Funding

Wellcome Trust 225221
6 · The paper itself

Abstract

backgroundChronic dry cough is a symptom of common lung conditions, can occur as a side-effect of angiotensin-converting enzyme inhibitors (ACEis), or may be unexplained. Despite the substantial health burden presented by chronic dry cough, its biological mechanisms remain unclear. We hypothesised shared genetic architecture between chronic dry cough and ACEi-induced cough and aimed to identify causal genes underlying both phenotypes.

methodsWe performed multi-ancestry genome-wide association studies (GWAS) of chronic dry cough and ACEi-induced cough, and a multi-trait GWAS of both phenotypes, utilising data from five cohort studies. Chronic dry cough was defined by questionnaire responses, and ACEi-induced cough by treatment switches or clinical diagnosis in electronic health records. We mapped putative causal genes and performed phenome-wide association studies (PheWAS) of associated variants, and polygenic scores for ACEi-induced cough, to identify pleiotropic effects.

resultsWe found seven novel genetic association signals reaching p<5×10

conclusionOur findings provide support for neuronal dysfunction underlying cough hypersensitivity in chronic dry cough and ACEi-induced cough, and identify diseases and traits associated with genetic predisposition to cough that could inform drug target discovery.

Indexed as

Angiotensin-Converting Enzyme InhibitorsCoughAdultAgedChronic DiseaseCohort StudiesFemaleGenetic Predisposition to DiseaseGenome-Wide Association StudyGenomicsHumansMaleMiddle AgedPhenotypePolymorphism, Single NucleotideAngiotensin-Converting Enzyme Inhibitors

Identifiers

PMID40675770
PMCPMC12461901

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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.