ArticleLipids in health and disease2024
Associations of lipids and lipid-modifying drug target genes with atrial fibrillation risk based on genomic data.
Article in Lipids in health and disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Systematic Identification of Therapeutic Targets and Repurposed Drugs for Stroke: From Genome Causal Analysis to Multilevel Validation.Journal of the American Heart Association · 2026Article
- Circulating cardiometabolic metabolite profiles associated with ambient air pollution and atrial fibrillation risk: a prospective cohort study.Cardiovascular diabetology · 2026Article
- Mendelian randomization study on the causal relationships among fasting blood glucose, plasma proteins, and squamous cell lung cancer.Discover oncology · 2025Article
- Multi-Omics Profiling of Lipid Variation and Regulatory Mechanisms in Poultry Breast Muscles.Animals : an open access journal from MDPI · 2025Article
- Inverse association between remnant cholesterol and risks of atrial fibrillation among patients with type 2 diabetes.Frontiers in endocrinology · 2025Article
- Lipoprotein(a) and Atrial Fibrillation: Mechanistic Insights and Therapeutic Approaches.International journal of medical sciences · 2025Review
- The functions of apolipoproteins and lipoproteins in health and disease.Molecular biomedicine · 2024Review
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Authors and funding
7 authors.
Funding
Abstract
backgroundThe causal associations of lipids and the drug target genes with atrial fibrillation (AF) risk remain obscure. We aimed to investigate the causal associations using genetic evidence.
methodsMendelian randomization (MR) analyses were conducted using summary-level genome-wide association studies (GWASs) in European and East Asian populations. Lipid profiles (low-density lipoprotein cholesterol, triglyceride, and lipoprotein[a]) and lipid-modifying drug target genes (3-hydroxy-3-methylglutaryl-CoA reductase, proprotein convertase subtilisin/kexin type 9, NPC1-like intracellular cholesterol transporter 1, apolipoprotein C3, angiopoietin-like 3, and lipoprotein[a]) were used as exposures. AF was used as an outcome. The inverse variance weighted method was applied as the primary method. Summary-data-based Mendelian randomization analyses were performed for further validation using expression quantitative trait loci data. Mediation analyses were conducted to explore the indirect effect of coronary heart disease.
resultsIn the European population, MR analyses demonstrated that elevated levels of lipoprotein(a) increased AF risk. Moreover, analyses focusing on drug targets revealed that the genetically proxied target gene LPA, which simulates the effects of drug intervention by reducing lipoprotein(a), exhibited an association with AF risk. This association was validated in independent datasets. There were no consistent and significant associations observed for other traits when analyzed in different datasets. This finding was also corroborated by Summary-data-based Mendelian randomization analyses between LPA and AF. Mediation analyses revealed that coronary heart disease plays a mediating role in this association. However, in the East Asian population, no statistically significant evidence was observed to support these associations.
conclusionsThis study provided genetic evidence that Lp(a) may be a causal factor for AF and that LPA may represent a promising pharmacological target for preventing AF in the European population.
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