{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Cheng PF"],"funding":["Noncommunicable Chronic Diseases-National Science and Technology Major Project"],"pagination":["97"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12181570"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["15(1)"],"pubmed_abstract":["Emerging evidence links gut microbiota (GM) to venous thromboembolism (VTE), deep vein thrombosis (DVT), and pulmonary embolism (PE), but causal insights are limited. Using two-sample Mendelian randomization (MR), we assessed causal effects of 211 GM taxa and 489 plasma metabolites on VTE/DVT/PE. Genetic instruments (single nucleotide polymorphism) for GM and metabolites were leveraged to infer causality, complemented by mediation and pathway analyses. Sixteen GM taxa (e.g., protective Firmicutes, Clostridia; risk-enhancing Bacteroidetes, Desulfovibrionaceae) and 40 metabolites showed causal associations with VTE/DVT/PE. Reverse MR identified 11 GM changes secondary to thrombosis. No pleiotropy or heterogeneity was detected. Ten metabolite-mediated pathways (e.g., arginine biosynthesis) bridged GM to thrombosis, suggesting GM-metabolite interactions as potential biomarkers for thrombotic risk stratification and prognosis."],"journal":["AMB Express"],"pubmed_title":["Gut microbiota, plasma metabolites, and venous thromboembolism: a Mendelian randomization study."],"pmcid":["PMC12181570"],"funding_grant_id":["2023ZD0502400"],"pubmed_authors":["Cheng PF","Wu JS","Li GM","Wang JX"],"additional_accession":[]},"is_claimable":false,"name":"Gut microbiota, plasma metabolites, and venous thromboembolism: a Mendelian randomization study.","description":"Emerging evidence links gut microbiota (GM) to venous thromboembolism (VTE), deep vein thrombosis (DVT), and pulmonary embolism (PE), but causal insights are limited. Using two-sample Mendelian randomization (MR), we assessed causal effects of 211 GM taxa and 489 plasma metabolites on VTE/DVT/PE. Genetic instruments (single nucleotide polymorphism) for GM and metabolites were leveraged to infer causality, complemented by mediation and pathway analyses. Sixteen GM taxa (e.g., protective Firmicutes, Clostridia; risk-enhancing Bacteroidetes, Desulfovibrionaceae) and 40 metabolites showed causal associations with VTE/DVT/PE. Reverse MR identified 11 GM changes secondary to thrombosis. No pleiotropy or heterogeneity was detected. Ten metabolite-mediated pathways (e.g., arginine biosynthesis) bridged GM to thrombosis, suggesting GM-metabolite interactions as potential biomarkers for thrombotic risk stratification and prognosis.","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Jun","modification":"2026-06-03T07:46:38.764Z","creation":"2026-04-26T03:10:05.607Z"},"accession":"S-EPMC12181570","cross_references":{"pubmed":["40540143"],"doi":["10.1186/s13568-025-01903-8"]}}