ArticleCommunications biology2023
Genome-wide cross-trait analysis and Mendelian randomization reveal a shared genetic etiology and causality between COVID-19 and venous thromboembolism.
Article in Communications biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- A Post-GWAS Analysis of the Shared Genetic Architecture Between COVID-19 and Coronary Artery Disease.International journal of molecular sciences · 2026Article
- Unraveling the genetic interplay and therapeutic potentials between major depressive disorder and metabolic syndrome: multi-ancestry and multi-trait genome-wide association analyses.BMC psychiatry · 2026Article
- Human genetics implicate thromboembolism in the pathogenesis of long COVID in individuals of European ancestry.Nature cardiovascular research · 2025Article
- Potential drug targets for peripheral artery disease identified through Mendelian randomization analysis.Thrombosis journal · 2025Article
- How the chromatin landscape influences nuclear morphology.Frontiers in cell and developmental biology · 2025Review
- Article
- Venous thromboembolism and severe COVID-19: a Mendelian randomization trial and transcriptomic analysis.Frontiers in immunology · 2024Article
- Novel mechanism of the COVID-19 associated coagulopathy (CAC) and vascular thromboembolism.Npj viruses · 2023Article
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Abstract
Venous thromboembolism occurs in up to one-third of patients with COVID-19. Venous thromboembolism and COVID-19 may share a common genetic architecture, which has not been clarified. To fill this gap, we leverage summary-level genetic data from the latest COVID-19 host genetics consortium and UK Biobank and examine the shared genetic etiology and causal relationship between COVID-19 and venous thromboembolism. The cross-trait and co-localization analyses identify 2, 3, and 4 shared loci between venous thromboembolism and severe COVID-19, COVID-19 hospitalization, SARS-CoV-2 infection respectively, which are mapped to ABO, ADAMTS13, FUT2 genes involved in coagulation functions. Enrichment analysis supports shared biological processes between COVID-19 and venous thromboembolism related to coagulation and immunity. Bi-directional Mendelian randomization suggests that venous thromboembolism was associated with higher risk of three COVID-19 traits, and SARS-CoV-2 infection was associated with a higher risk of venous thromboembolism. Our study provides timely evidence for the genetic etiology between COVID-19 and venous thromboembolism (VTE). Our findings contribute to the understanding of COVID-19 and VTE etiology and provide insights into the prevention and comorbidity management of COVID-19.
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