SynthesisCirculation. Cardiovascular genetics2014
Multiple associated variants increase the heritability explained for plasma lipids and coronary artery disease.
Synthesis in Circulation. Cardiovascular genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed.
- A multi-trait genome-wide association study of coronary artery disease and subclinical atherosclerosis traits.Research square · 2025Article
- A Multiplexed Quantitative Proteomics Approach to the Human Plasma Protein Signature.Biomedicines · 2024Article
- Evaluation of the Relationship between Family History and Occurrence, Anatomical Location, and Extent of Coronary Artery Disease among Patients Undergoing Coronary Angiography.Medical journal of the Islamic Republic of Iran · 2023Article
- Article
- Interpreting coronary artery disease GWAS results: A functional genomics approach assessing biological significance.PloS one · 2022Article
- Lipid Phenotypes and DNA Methylation: a Review of the Literature.Current atherosclerosis reports · 2021Review
- Genomic profiling of human vascular cells identifies TWIST1 as a causal gene for common vascular diseases.PLoS genetics · 2020Article
- Inferring the Nature of Missing Heritability in Human Traits Using Data from the GWAS Catalog.Genetics · 2019Article
- Functionally oriented analysis of cardiometabolic traits in a trans-ethnic sample.Human molecular genetics · 2019Article
- Generalized multifactor dimensionality reduction approaches to identification of genetic interactions underlying ordinal traits.Genetic epidemiology · 2019Article
- Multiple rare and common variants in APOB gene locus associated with oxidatively modified low-density lipoprotein levels.PloS one · 2019Article
- Global genetic diversity of human apolipoproteins and effects on cardiovascular disease risk.Journal of lipid research · 2018Article
- A large electronic-health-record-based genome-wide study of serum lipids.Nature genetics · 2018Article
- Genetic architecture of lipid traits in the Hispanic community health study/study of Latinos.Lipids in health and disease · 2017Article
- Clinical Perspectives of Genetic Analyses on Dyslipidemia and Coronary Artery Disease.Journal of atherosclerosis and thrombosis · 2017Review
- Heritability of Vascular Structure and Function: A Parent-Child Study.Journal of the American Heart Association · 2017Article
- Genome-wide association analyses using electronic health records identify new loci influencing blood pressure variation.Nature genetics · 2017Article
- Genetic variants in CETP increase risk of intracerebral hemorrhage.Annals of neurology · 2016Article
- Analysis with the exome array identifies multiple new independent variants in lipid loci.Human molecular genetics · 2016Article
- Sixteen new lung function signals identified through 1000 Genomes Project reference panel imputation.Nature communications · 2015Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
backgroundPlasma lipid levels as well as coronary artery disease (CAD) have been shown to be highly heritable with estimates ranging from 40% to 60%. However, top variants detected by large-scale genome-wide association studies explain only a fraction of the total variance in plasma lipid phenotypes and CAD. METHODS AND
resultsWe performed a conditional and joint association analysis using summary-level statistics from 2 large genome-wide association meta-analyses: the Global Lipids Genetics Consortium (GLGC) study, and the Coronary Artery Disease Genome-Wide Replication and Meta-Analysis (CARDIoGRAM) study. There were 100 184 individuals from 46 GLGC studies for plasma lipids, and 22 233 cases and 64 762 controls from 14 studies for CAD. We detected several loci where multiple independent single-nucleotide polymorphisms were associated with lipid traits within a locus (12 out of 33 loci for high-density lipoprotein cholesterol, 10 of 35 loci for low-density lipoprotein cholesterol, 13 of 44 loci for total cholesterol, and 8 of 28 loci for triglycerides), reaching genome-wide significance (P<5×10(-8)), nearly doubling the heritability explained by genome-wide association studies (from 3.6 to 7.6% for high-density lipoprotein cholesterol, from 5.0 to 8.8% for low-density lipoprotein cholesterol, from 5.5 to 8.8% for total cholesterol, and from 5.7 to 8.5% for triglycerides). Multiple single-nucleotide polymorphisms were also associated with CAD (3 of 15 loci; an increase from 9.6% to 11.4% of heritability explained).
conclusionsThese results demonstrate that a portion of the missing heritability for lipid traits and CAD can be explained by multiple variants at each locus.
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