ArticleFrontiers in nutrition2024
Causality of blood metabolites and metabolic pathways on peripheral arteriosclerosis: a Mendelian randomization study.
Article in Frontiers in nutrition, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Dissecting causal relationships between inflammatory factors, plasma metabolites, and nonalcoholic fatty liver disease: a mediating Mendelian randomization study.European journal of gastroenterology & hepatology · 2026Article
- The Causal Association between Plasma Metabolites-Mediated Immune Cells and Myocardial Infarction: A Mendelian Randomization Study.Arquivos brasileiros de cardiologia · 2026Article
- SIRT6 Lysine-Demyristoylates ATF2 to Ameliorate Vascular Injury via PRKCD/VE-Cadherin Pathway Regulating Vascular Endothelial Barrier.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Exploring BMI's mediating influence on cardiovascular risk correlations with the triglyceride-glucose index: using NHANES and CHARLS cohorts.Frontiers in cardiovascular medicine · 2025Article
- Molecular mechanisms and therapeutic progress in atherosclerosis: bridging immune inflammation and precision medicine.Frontiers in immunology · 2025Review
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Abstract
Background: Peripheral arteriosclerosis is caused by any atherosclerosis outside the heart and brain. However, the underlying biological mechanisms are not fully understood. This study aims to explore the causal relationship between blood metabolites and peripheral arteriosclerosis. Methods: A Mendelian randomization (MR) analysis was implemented to estimate the causality of blood metabolites on peripheral arteriosclerosis. A genome-wide association study (GWAS) of 1,400 metabolites was used as the exposure, whereas two different GWAS datasets of peripheral arteriosclerosis were the outcomes. Inverse-variance weighted (IVW) was the main analysis of causal analysis. MR-Egger, the simple mode, weighted median and weighted mode were used to increase the stability and robustness of the results. Cochran Q test, MR-Egger intercept test, the funnel plot, and MR-Pleiotropy RESidual Sum and Outlier were used for sensitivity analyses. Furthermore, metabolic pathway enrichment analysis was performed using MetaboAnalyst5.0. Results: In this MR study, eight blood metabolites have a strong causal relationship with peripheral arteriosclerosis, including 1-myristoyl-2-arachidonoyl-GPC (14:0/20:4), 1-palmitoyl-2-arachidonoyl-gpc (16:0/20:4n6), 1-(1-enyl-stearoyl)-2-arachidonoyl-GPE, 1-palmitoyl-2-dihomo-linolenoyl-GPC, Gamma-glutamylleucine, Deoxycholic acid glucuronide and two named X- (X-24546, X-26111). In addition, five important metabolic pathways in peripheral arteriosclerosis were identified through metabolic pathway analysis. Conclusion: This study provides evidence for the causal relationship between blood metabolites and peripheral arteriosclerosis, and these eight blood metabolites provide new perspectives for screening and prevention of peripheral arteriosclerosis in the future.
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