ArticleAmerican journal of human genetics1998
Families with familial combined hyperlipidemia and families enriched for coronary artery disease share genetic determinants for the atherogenic lipoprotein phenotype.
Article in American journal of human genetics, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
11 citing papers in PubMed, 68 citations in OpenAlex.
- 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
- Zebrafish as an Emerging Model for Dyslipidemia and Associated Diseases.Journal of lipid and atherosclerosis · 2021Review
- The genetics of familial combined hyperlipidaemia.Nature reviews. Endocrinology · 2012Review
- Review
- Ion mobility analysis of lipoprotein subfractions identifies three independent axes of cardiovascular risk.Arteriosclerosis, thrombosis, and vascular biology · 2009Article
- A genome-wide linkage scan identifies multiple chromosomal regions influencing serum lipid levels in the population on the Samoan islands.Journal of lipid research · 2008Article
- Genetic studies on the APOA1-C3-A5 gene cluster in Asian Indians with premature coronary artery disease.Lipids in health and disease · 2008Article
- An apolipoprotein A-V gene SNP is associated with marked hypertriglyceridemia among Asian-American patients.Journal of lipid research · 2008Article
- A genome scan for familial combined hyperlipidemia reveals evidence of linkage with a locus on chromosome 11.American journal of human genetics · 1999Article
- Genetics of familial combined hyperlipidemia.Current atherosclerosis reports · 1999Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
Abstract
Small, dense LDL particles consistently have been associated with hypertriglyceridemia, premature coronary artery disease (CAD), and familial combined hyperlipidemia (FCH). Previously, we have observed linkage of LDL particle size with four separate candidate-gene loci in a study of families enriched for CAD. These loci contain the genes for manganese superoxide dismutase (MnSOD), on chromosome 6q; for apolipoprotein AI-CIII-AIV, on chromosome 11q; for cholesteryl ester transfer protein (CETP) and lecithin:cholesterol acyltransferase (LCAT), on chromosome 16q; and for the LDL receptor (LDLR), on chromosome 19p. We have now tested whether these loci also contribute to LDL particle size in families ascertained for FCH. The members of 18 families (481 individuals) were typed for genetic markers at the four loci, and linkage to LDL particle size was assessed by nonparametric sib-pair linkage analysis. The presence of small, dense LDL (pattern B) was much more frequent in the FCH probands (39%) than in the spouse controls (4%). Evidence for linkage was observed at the MnSOD (P=.02), CETP/LCAT (P=.03), and apolipoprotein AI-CIII-AIV loci (P=.005) but not at the LDLR locus. We conclude that there is a genetically based association between FCH and small, dense LDL and that the genetic determinants for LDL particle size are shared, at least in part, among FCH families and the more general population at risk for CAD.
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Registered trials
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