ArticleBMC genetics2003
Search for genetic factors predisposing to atherogenic dyslipidemia.
Article in BMC genetics, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Association ofInternational journal of clinical and experimental pathology · 2017Article
- Association of the ARL15 rs6450176 SNP and serum lipid levels in the Jing and Han populations.International journal of clinical and experimental pathology · 2015Article
- Genome-wide linkage scan identifies two novel genetic loci for coronary artery disease: in GeneQuest families.PloS one · 2014Article
- Genetic copy number variants in myocardial infarction patients with hyperlipidemia.BMC genomics · 2011Article
- Fine mapping and association studies of a high-density lipoprotein cholesterol linkage region on chromosome 16 in French-Canadian subjects.European journal of human genetics : EJHG · 2010Article
- Empirically derived phenotypic subgroups - qualitative and quantitative trait analyses.BMC genetics · 2003Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAtherogenic dyslipidemia (AD) is a common feature in persons with premature coronary heart disease. While several linkage studies have been carried out to dissect the genetic etiology of lipid levels, few have investigated the AD lipid triad comprising elevated serum triglyceride, small low density lipoprotein (LDL) particles, and reduced high density lipoprotein (HDL) cholesterol levels. Here we report the results of a whole-genome screen for AD using the Framingham Heart Study population.
resultsOur analyses provide some evidence for linkage to AD on chromosomes 1q31, 3q29, 10q26, 14p12, 14q13, 16q24, 18p11, and 19q13.
conclusionAD susceptibility is modulated by multiple genes in different chromosomes. Our study confirms results from other populations and suggests new areas of potential importance.
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