Evidence map›Paper›PMID 18242618›Full record

ArticleAtherosclerosis2008

Functional significance of lipoprotein lipase HindIII polymorphism associated with the risk of coronary artery disease.

Qi Chen, Hamid Razzaghi, F Yesim Demirci, M Ilyas Kamboh

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Atherosclerosis, 2008. 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 14% 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, 41 citations in OpenAlex.

  1. Lipoprotein Lipase (LPL) Polymorphism and the Risk of Coronary Artery Disease: A Meta-Analysis.International journal of environmental research and public health · 2017
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  4. Association of Lipoprotein Lipase (International journal of molecular sciences · 2025
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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

4 authors at 1 institution in 1 country.

Qi ChenDepartment of Human Genetics, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA 15261, USA.
Hamid Razzaghi
F Yesim Demirci
M Ilyas Kamboh
University of Pittsburgh · US

Funding

Functional Characterization-Lipoprotein Lipase MutationsR01HL070169 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KAMBOH, M. ILYAS · 2003 to 2006
$1.4M
NHLBI NIH HHS HL 070169NHLBI NIH HHS R01 HL070169
6 · The paper itself

Abstract

Lipoprotein lipase (LPL) plays a pivotal role in lipid metabolism by hydrolyzing triglyceride (TG)-rich lipoprotein particles. Abnormalities in normal LPL function are associated with the risk of coronary artery disease (CAD). A number of genetic variants have been identified in the LPL gene that affects different functions of the LPL protein. A common HindIII polymorphism in intron 8 (T/G) of the LPL gene has been found to be associated with altered plasma TG and HDL-cholesterol, and CAD risk in several studies, but its functional significance is unknown. It has been shown that certain intronic sequence contain regulatory elements that are important for transcription and translational regulation of a gene. In this study we tested the hypothesis that this polymorphism affects the binding site of a transcription factor that regulates the transcription of LPL gene. Electrophoretic mobility shift assays (EMSAs) revealed that the HindIII site binds to a transcription factor and that the mutant allele has lower binding affinity than the wild type allele. Transcription assays containing the entire intron 8 sequence along with full-length human LPL promoter were carried out in COS-1 and human vascular smooth muscle cells. The mutant allele was associated with significantly decreased luciferase expression level compared to the wild type allele in both the muscle (3.394+/-0.022 vs. 4.184+/-0.028; P=4.7 x 10(-6)) and COS-1 (11.603+/-0.409 vs. 14.373+/-1.096; P<0.0001) cells. In conclusion, this study demonstrates for the first time that the polymorphic HindIII site in the LPL gene is functional because it affects the binding of a transcription factor and it also has an impact on LPL expression.

Indexed as

AnimalsChlorocebus aethiopsCoronary Artery DiseaseCOS CellsElectrophoretic Mobility Shift AssayGenetic Predisposition to DiseaseHumansIntronsLipoprotein LipaseMuscle, Smooth, VascularMyocytes, Smooth MusclePolymorphism, Restriction Fragment LengthPolymorphism, Single NucleotideSite-Specific DNA-Methyltransferase (Adenine-Specific)Transcription FactorsDNA modification methylase HindIIILipoprotein LipaseSite-Specific DNA-Methyltransferase (Adenine-Specific)Transcription Factors

Identifiers

PMID18242618
PMCPMC2603421
OpenAlexW2003605422

What OpenQuestion holds

Textmetadata
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.