ArticlePolish journal of microbiology2025
Causal Relationship between Gut Microbiota and Pulmonary Embolism: An Analysis Using Mendelian Randomization.
Article in Polish journal of microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
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Who cites it
3 citing papers in PubMed.
- Genetic and biological determinants of pulmonary embolism: Insights from Mendelian randomization studies.World journal of experimental medicine · 2026Review
- Gut Microbiota Dysbiosis and Risk of Venous Thromboembolism: A Systematic Review.Microorganisms · 2026Review
- Venous Thromboembolism and Gut Dysbiosis: Mechanistic Links Between Endotoxemia, Microbial Metabolites, and Thromboinflammation.Nutrients · 2026Review
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Authors and funding
7 authors.
Funding
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Abstract
Previous research has demonstrated a connection between an unbalanced gut microbiome (GM) and lung diseases, suggesting that gut bacteria may affect lung health through the "gut-lung" axis. However, the direct connection between GM and pulmonary embolism (PE) is unclear. Mendelian randomization studies were used to investigate GM's genetic relationship with PE. A total of 18,340 independent genewide association studies (GWAS) yielded single nucleotide polymorphisms (SNPs) linked to the GM, which were then used as instrumental variables in a multiple regression analysis (MR) to examine the effect of GM on the risk of PE within the IEU Open GWAS project, which included 2,118 PE cases and 359,076 controls. The principal analytical methodology utilized in this research was inverse variance weighting (IVW), complemented by assessments for pleiotropy and heterogeneity to confirm the results' resilience. The findings of this study are predominantly derived from the IVW method, providing evidence for causal associations between four distinct genera of GM and the risk of PE. Specifically, our analysis suggests that
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