ArticleArteriosclerosis, thrombosis, and vascular biology2004
Linkage and association between distinct variants of the APOA1/C3/A4/A5 gene cluster and familial combined hyperlipidemia.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 104 citations in OpenAlex.
- Apolipoprotein A5 gene variants and the risk of coronary heart disease: a case‑control study and meta‑analysis.Molecular medicine reports · 2013Pooled it
- Genetic variation in lean body mass, changes of appetite and weight loss in response to diet interventions: The POUNDS Lost trial.Diabetes, obesity & metabolism · 2020Trial
- Plasma apolipoprotein A5 and triglycerides in type 2 diabetes.Diabetologia · 2006Trial
- Familial Combined Hyperlipidemia: Myth or Reality?Current atherosclerosis reports · 2025Review
- Current Data and New Insights into the Genetic Factors of Atherogenic Dyslipidemia Associated with Metabolic Syndrome.Diagnostics (Basel, Switzerland) · 2023Review
- Etiologic Puzzle of Coronary Artery Disease: How Important Is Genetic Component?Life (Basel, Switzerland) · 2022Review
- Genetic Regulatory Networks of Apolipoproteins and Associated Medical Risks.Frontiers in cardiovascular medicine · 2021Review
- Apolipoprotein C1: Its Pleiotropic Effects in Lipid Metabolism and Beyond.International journal of molecular sciences · 2019Review
- Quantitative trait loci at the 11q23.3 chromosomal region related to dyslipidemia in the population of Andhra Pradesh, India.Lipids in health and disease · 2017Article
- GLADIATOR: a global approach for elucidating disease modules.Genome medicine · 2017Article
- Genetic determinants of clinical heterogeneity of the coronary artery disease in the population of Hyderabad, India.Human genomics · 2017Article
- Interactions between Genetics and Sugar-Sweetened Beverage Consumption on Health Outcomes: A Review of Gene-Diet Interaction Studies.Frontiers in endocrinology · 2017Review
- Genetics of coronary heart disease with reference to ApoAI-CIII-AIV gene region.World journal of cardiology · 2014Review
- Article
- CDKN2B expression in adipose tissue of familial combined hyperlipidemia patients.Journal of lipid research · 2013Article
- The genetics of familial combined hyperlipidaemia.Nature reviews. Endocrinology · 2012Review
- Haplotype analysis of Apo AI-CIII-AIV gene cluster and lipids level: Tehran Lipid and Glucose Study.Endocrine · 2012Article
- Apolipoprotein A1/C3/A5 haplotypes and serum lipid levels.Lipids in health and disease · 2011Article
- Stepwise positive association between APOA5 minor allele frequencies and increasing plasma triglyceride quartiles in random patients with hypertriglyceridemia of unclarified origin.Pathology oncology research : POR · 2011Article
- FABP4 plasma levels are increased in familial combined hyperlipidemia.Journal of lipid research · 2010Article
Corrections and comments
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Authors and funding
14 authors at 6 institutions in 2 countries.
Funding
Abstract
objectiveCombined hyperlipidemia is a common disorder, characterized by a highly atherogenic lipoprotein profile and a substantially increased risk of coronary heart disease. The purpose of this study was to establish whether variations of apolipoprotein A5 (APOA5), a newly discovered gene of lipid metabolism located 30 kbp downstream of the APOA1/C3/A4 gene cluster, contributes to the transmission of familial combined hyperlipidemia (FCHL). METHODS AND
resultsWe performed linkage and association tests on 128 families. Two independent alleles, APOA5c.56G and APOC3c.386G, of the APOA1/C3/A4/A5 gene cluster were overtransmitted in FCHL (P=0.004 and 0.007, respectively). This was paired with reduced transmission of the common APOA1/C3/A4/A5 haplotype (frequency 0.4461) to affected subjects (P=0.012). The APOA5c.56G genotype accounted for 7.3% to 13.8% of the variance in plasma triglyceride levels in probands (P<0.004). The APOC3c.386G genotypes accounted for 4.4% to 5.1% of the variance in triglyceride levels in FCHL spouses (P<0.007), suggesting that this allele marks a FCHL quantitative trait as well as representing a susceptibility locus for the condition.
conclusionsA combined linkage and association analysis establishes that variation at the APOA1/C3/A4/A5 gene cluster contributes to FCHL transmission in a substantial proportion of northern European families.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.