Evidence map›Paper›PMID 40247961›Full record

ArticleERJ open research2025

Polygenic risk of idiopathic pulmonary fibrosis and COVID-19 severity.

Beatriz Guillen-Guio, Itahisa Marcelino-Rodriguez, José Miguel Lorenzo-Salazar, Olivia C Leavy, Richard J Allen, Ericka N Pompa-Mera, José A Riancho, Augusto Rojas-Martinez, Pablo Lapunzina, Ángel Carracedo and 2 more

Abstract read
In one paragraph

Article in ERJ open research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Review
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

12 authors.

Beatriz Guillen-GuioDepartment of Population Health Sciences, University of Leicester, Leicester, UK.ORCID https://orcid.org/0000-0002-3703-1738
Itahisa Marcelino-RodriguezResearch Unit, Hospital Universitario Nuestra Señora de Candelaria, Instituto de Investigación Sanitaria de Canarias, Santa Cruz de Tenerife, Spain.
José Miguel Lorenzo-SalazarGenomics Division, Instituto Tecnológico y de Energías Renovables, Santa Cruz de Tenerife, Spain.ORCID https://orcid.org/0000-0002-5135-2861
Olivia C LeavyDepartment of Population Health Sciences, University of Leicester, Leicester, UK.
Richard J AllenDepartment of Population Health Sciences, University of Leicester, Leicester, UK.
Ericka N Pompa-MeraUnidad de Investigación Médica en Enfermedades Infecciosas y Parasitarias, Hospital de Pediatría, Centro Médico Nacional s.XXI, Instituto Mexicano del Seguro Social, Mexico City, Mexico.
José A RianchoIDIVAL, Cantabria, Spain.
Augusto Rojas-MartinezTecnologico de Monterrey, The Institute for Obesity Research and Escuela de Medicina y Ciencias de la Salud, Monterrey, Mexico.
Pablo LapunzinaCentro de Investigación Biomédica en Red de Enfermedades Raras, Instituto de Salud Carlos III, Madrid, Spain.
Ángel CarracedoCentro de Investigación Biomédica en Red de Enfermedades Raras, Instituto de Salud Carlos III, Madrid, Spain.
Louise V WainDepartment of Population Health Sciences, University of Leicester, Leicester, UK.ORCID https://orcid.org/0000-0003-4951-1867
Carlos FloresResearch Unit, Hospital Universitario Nuestra Señora de Candelaria, Instituto de Investigación Sanitaria de Canarias, Santa Cruz de Tenerife, Spain.

Funding

Wellcome Trust
6 · The paper itself

Abstract

Background: A shared genetic component between coronavirus disease 2019 (COVID-19) and idiopathic pulmonary fibrosis (IPF) has been described based on analyses of individual risk variants. Here we used a whole-genome polygenic risk score (PRS) approach to further evaluate age- and sex-stratified genetic overlap between IPF and severe COVID-19 to give insight into shared biological mechanisms that might both inform therapeutic strategies for both diseases. Methods: We used results from the largest genome-wide association study of clinically defined IPF risk (4125 cases/20 464 controls) and individual-level data from the SCOURGE European study of COVID-19 (5968 cases/9056 controls). We calculated IPF PRSs and assessed their association with COVID-19 severity, stratified by age and sex. We performed replication in an independent dataset of Latin-American patients (1625 cases/1887 controls). Enrichment and pathway-specific PRS analyses were performed to study biological pathways associated with COVID-19 severity. Results: IPF PRSs were significantly associated with COVID-19 hospitalisation and severe illness in Europeans and replicated in a Latin-American cohort. The strongest association was found in <60 years patients, especially among younger males (p=6.39×10 Conclusions: The study indicates age and sex-dependent genome-wide genetic overlap between IPF and severe COVID-19 and highlights specific shared biological mechanisms underlying both conditions. This could also imply that individuals with a high IPF genetic risk are at an overall increased risk of developing lung sequelae resulting from severe COVID-19.

Identifiers

PMID40247961
PMCPMC12004260

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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.