ArticleEBioMedicine2021
Shared genetic etiology between idiopathic pulmonary fibrosis and COVID-19 severity.
Article in EBioMedicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 5 of them syntheses that pooled it.
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Who cites it
61 citing papers in PubMed, 5 syntheses or guidelines pooled it, 96 citations in OpenAlex.
- Common and rare variant analyses reveal genetic factors underlying idiopathic pulmonary fibrosis and its shared aetiology with severe COVID-19.EBioMedicine · 2025Pooled it
- Systematic review of overlapping microRNA patterns in COVID-19 and idiopathic pulmonary fibrosis.Respiratory research · 2023Pooled it
- AAmerican journal of respiratory and critical care medicine · 2022Pooled it
- Pooled it
- Identifying factors contributing to increased susceptibility to COVID-19 risk: a systematic review of Mendelian randomization studies.International journal of epidemiology · 2022Pooled it
- Disentangling Shared and Differential Genetic Architectures Between COVID-19 and Other Respiratory Disorders-A Genome-Wide Multi-Omics Framework.International journal of molecular sciences · 2026Article
- Next-Generation Sequencing in Pulmonary Fibrosis: Translational Promise and Current Clinical Limitations.Current issues in molecular biology · 2026Review
- Pulmonary fibrosis after COVID-19 is characterized by airway abnormalities and elevated club cell secretory protein-16.JCI insight · 2026Article
- Decoding the shared genetic liability of lower respiratory tract infections via genomic structural equation modeling.BMC pulmonary medicine · 2026Article
- Causal and shared genetic insights into severe COVID-19 and idiopathic pulmonary fibrosis.iScience · 2026Article
- Age-dependent Genetic Risk in Pulmonary Fibrosis Patients and Relatives.medRxiv : the preprint server for health sciences · 2026Article
- Integrated Mendelian Randomization and Single-Cell RNA Sequencing Analyses Reveal Lactate Metabolism as a Key Pathway in COVID-19-Induced Pulmonary Fibrosis.Canadian respiratory journal · 2026Article
- Unveiling the secret of cellular metamorphosis: the crucial role of EndMT mechanisms in COVID-19-induced pulmonary fibrosis.Inflammopharmacology · 2025Review
- Scars from the pandemic: understanding post-COVID-19 interstitial lung disease.Breathe (Sheffield, England) · 2025Review
- A Computable Electronic Health Record ARDS Classifier and the Association Between theCHEST critical care · 2025Article
- Stratifying GAP Stages by MUC5B rs35705950 T-Allele Carriage Refines Survival Prediction in IPF.Lung · 2025Article
- Associations of Prepandemic Lung Function and Structure with COVID-19 Outcomes: The C4R Study.American journal of respiratory and critical care medicine · 2025Article
- Polygenic risk of idiopathic pulmonary fibrosis and COVID-19 severity.ERJ open research · 2025Article
- Role of IPF genetic risk loci in post-COVID-19 lung abnormalities: a cohort study.BMJ open respiratory research · 2025Article
- Imperfect wound healing sets the stage for chronic diseases.Science (New York, N.Y.) · 2024Review
1 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 6 institutions in 5 countries.
Funding
Abstract
backgroundIdiopathic pulmonary fibrosis (IPF) is a complex lung disease, characterized by progressive lung scarring. Severe COVID-19 is associated with substantial pneumonitis and has a number of shared major risk factors with IPF. This study aimed to determine the genetic correlation between IPF and severe COVID-19 and assess a potential causal role of genetically increased risk of IPF on COVID-19 severity.
methodsThe genetic correlation between IPF and COVID-19 severity was estimated with linkage disequilibrium (LD) score regression. We performed a Mendelian randomization (MR) study for IPF causality in COVID-19. Genetic variants associated with IPF susceptibility (P<5 × 10
findingsWe detected a positive genetic correlation of IPF with COVID-19 severity (rg=0·31 [95% CI 0·04-0·57], P = 0·023). The MR estimates for severe COVID-19 did not reveal any genetic association (OR 1·05, [95% CI 0·92-1·20], P = 0·43). However, outlier analysis revealed that the IPF risk allele rs35705950 at MUC5B had a different effect compared with the other variants. When rs35705950 was excluded, MR results provided evidence that genetically increased risk of IPF has a causal effect on COVID-19 severity (OR 1·21, [95% CI 1·06-1·38], P = 4·24 × 10
interpretationThe strongest genetic determinant of IPF, rs35705950 at MUC5B, seems to confer protection against COVID-19, whereas the combined effect of all other IPF risk loci seem to confer risk of COVID-19 severity. The observed effect of rs35705950 could either be due to protective effects of mucin over-production on the airways or a consequence of selection bias due to (1) a patient group that is heavily enriched for the rs35705950 T undertaking strict self-isolation and/or (2) due to survival bias of the rs35705950 non-IPF risk allele carriers. Due to the diverse impact of IPF causal variants on SARS-CoV-2 infection, with a possible selection bias as an explanation, further investigation is needed to address this apparent paradox between variance at MUC5B and other IPF genetic risk factors.
fundingNovo Nordisk Foundation and Oak Foundation.
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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 Socratic graph.