Evidence map›Paper›PMID 19951432›Full record

ArticleLipids in health and disease2009

Analysis of recently identified dyslipidemia alleles reveals two loci that contribute to risk for carotid artery disease.

James Ronald, Ramakrishnan Rajagopalan, Jane E Ranchalis, Julieann K Marshall, Thomas S Hatsukami, Patrick J Heagerty, Gail P Jarvik

Open access · goldAbstract read
In one paragraph

Article in Lipids in health and disease, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 2 pooled it
1.9field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 2 syntheses or guidelines pooled it, 35 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  18. Evidence of how rs7575840 influences apolipoprotein B-containing lipid particles.Arteriosclerosis, thrombosis, and vascular biology · 2011
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

James RonaldDepartment of Medicine, Division of Medical Genetics, University of Washington, Seattle, WA, USA. jscr@u.washington.edu
Ramakrishnan Rajagopalan
Jane E Ranchalis
Julieann K Marshall
Thomas S Hatsukami
Patrick J Heagerty
Gail P Jarvik
University of Washington Medical Center · USUniversity of Washington · US

Funding

Serum Amyloid and Inflammation in AtherogenesisP01HL030086 · NHLBI · UNIVERSITY OF WASHINGTON · PI HEINECKE, JAY W · 1985 to 2009
$14.7M
Prediction and Progression of Carotid Artery DiseaseR01HL067406 · NHLBI · UNIVERSITY OF WASHINGTON · PI JARVIK, GAIL PAIRITZ · 2002 to 2009
$5.1M
NHLBI NIH HHS P01 HL30086NHLBI NIH HHS R01 HL67406
6 · The paper itself

Abstract

backgroundGenome-wide association studies have identified numerous single nucleotide polymorphisms (SNPs) affecting high density lipoprotein (HDL) or low density lipoprotein (LDL) cholesterol levels; these SNPs may contribute to the genetic basis of vascular diseases.

resultsWe assessed the impact of 34 SNPs at 23 loci on dyslipidemia, key lipid sub-phenotypes, and severe carotid artery disease (CAAD) in a case-control cohort. The effects of these SNPs on HDL and LDL were consistent with those previously reported, and we provide unbiased estimates of the percent variance in HDL (3.9%) and LDL (3.3%) explained by genetic risk scores. We assessed the effects of these SNPs on HDL subfractions, apolipoprotein A-1, LDL buoyancy, apolipoprotein B, and lipoprotein (a) and found that rs646776 predicts apolipoprotein B level while rs2075650 predicts LDL buoyancy. Finally, we tested the role of these SNPs in conferring risk for ultrasonographically documented CAAD stenosis status. We found that two loci, chromosome 1p13.3 near CELSR2 and PSRC1 which contains rs646776, and 19q13.2 near TOMM40 and APOE which contains rs2075650, harbor risk alleles for CAAD.

conclusionOur analysis of 34 SNPs contributing to dyslipidemia at 23 loci suggests that genetic variation in the 1p13.3 region may increase risk of CAAD by increasing LDL particle number, whereas variation in the 19q13.2 region may increase CAAD risk by promoting formation of smaller, denser LDL particles.

Indexed as

AllelesAgedCarotid Artery DiseasesCholesterol, HDLCholesterol, LDLChromosomes, Human, Pair 1Chromosomes, Human, Pair 19DyslipidemiasGenetic LociGenetic Predisposition to DiseaseHumansLinkage DisequilibriumMiddle AgedPolymorphism, Single NucleotideRisk FactorsCholesterol, HDLCholesterol, LDL

Identifiers

PMID19951432
PMCPMC2794863
OpenAlexW2150847484

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.