<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>104(36)</volume><submitter>Huang L</submitter><pubmed_abstract>Coronary artery atherosclerosis (CAA) stands as a prominent etiological contributor to global cardiovascular morbidity and mortality. Its pathogenesis entails intricate interplays among genetic predisposition, environmental factors, and lifestyle determinants. Trace elements, though necessitated in minuscule quantities, have emerged as potential modulators of CAA progression, yet their exact impact remains unclear. We utilized Mendelian randomization (MR) analysis, employing genetic variants as instrumental variables to investigate the causal relationship between trace element levels and CAA. This study conducted a dual-sample MR analysis using data extracted from genome-wide association studies (GWAS) and the FinnGen database. To assess the statistical significance of these associations, </pubmed_abstract><journal>Medicine</journal><pagination>e44244</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12419359</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Vitamin A and vitamin B12 levels and coronary artery atherosclerosis: Univariate and multivariate Mendelian randomization analysis.</pubmed_title><pmcid>PMC12419359</pmcid><pubmed_authors>Li H</pubmed_authors><pubmed_authors>Lin Q</pubmed_authors><pubmed_authors>Huang L</pubmed_authors><pubmed_authors>Shi J</pubmed_authors></additional><is_claimable>false</is_claimable><name>Vitamin A and vitamin B12 levels and coronary artery atherosclerosis: Univariate and multivariate Mendelian randomization analysis.</name><description>Coronary artery atherosclerosis (CAA) stands as a prominent etiological contributor to global cardiovascular morbidity and mortality. Its pathogenesis entails intricate interplays among genetic predisposition, environmental factors, and lifestyle determinants. Trace elements, though necessitated in minuscule quantities, have emerged as potential modulators of CAA progression, yet their exact impact remains unclear. We utilized Mendelian randomization (MR) analysis, employing genetic variants as instrumental variables to investigate the causal relationship between trace element levels and CAA. This study conducted a dual-sample MR analysis using data extracted from genome-wide association studies (GWAS) and the FinnGen database. To assess the statistical significance of these associations, </description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Sep</publication><modification>2026-06-02T17:38:00.514Z</modification><creation>2026-04-18T03:11:55.352Z</creation></dates><accession>S-EPMC12419359</accession><cross_references><pubmed>40922374</pubmed><doi>10.1097/MD.0000000000044244</doi></cross_references></HashMap>