Evidence map›Paper›PMID 15861005›Full record

ReviewCurrent opinion in cardiology2005

Molecular genetics of coronary artery disease.

Qing Wang

Abstract readReview
In one paragraph

Review in Current opinion in cardiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed, 3 pooled it
3.4field-weighted citation impact, top 7% 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

65 citing papers in PubMed, 3 syntheses or guidelines pooled it, 194 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. Association ofGenes · 2023
    Article
  6. Article
  7. Polymorphism of rs599839 in theJournal of cardiovascular and thoracic research · 2023
    Article
  8. Distinct Features of Vascular Diseases in COVID-19.Journal of inflammation research · 2023
    Review
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  20. Association ofOncotarget · 2017
    Article

5 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 2 countries.

Qing WangDepartment of Molecular Cardiology, Lerner Research Institute, The Cleveland Clinic Foundation, Cleveland, OH 44195, USA. wangq2@ccf.org
Bridge University · SS

Funding

Molecular Mechanisms of Cardiac ArrhythmiasR01HL066251 · NHLBI · CLEVELAND CLINIC LERNER COL/MED-CWRU · PI WANG, QING KENNETH · 2002 to 2005
$1.7M
GENES FOR VASCULAR MORPHOGENESIS: A GENETIC APPROACHR01HL065630 · NHLBI · CLEVELAND CLINIC FOUNDATION · PI WANG, QING KENNETH · 2000 to 2003
$1.4M
Molecular Determinants of Coronary Artery DiseaseR01HL073817 · NHLBI · CLEVELAND CLINIC LERNER COL/MED-CWRU · PI WANG, QING KENNETH · 2004 to 2004
$189k
NHLBI NIH HHS R01 HL065630NHLBI NIH HHS R01 HL066251NHLBI NIH HHS R01 HL073817NHLBI NIH HHS R01 HL65630NHLBI NIH HHS R01 HL66251NHLBI NIH HHS R01 HL73817
6 · The paper itself

Abstract

purpose of reviewCoronary artery disease, including its most severe complication myocardial infarction, is the leading cause of death; however, its genetic studies lag behind other diseases. Many advances have recently been made, however, and these are reviewed here. RECENT

findingsPositional cloning based on genome-wide linkage analysis with large families identified the first non - lipid-related disease-causing gene, MEF2A (encoding a transcriptional factor), for coronary artery disease and myocardiaI infarction. The MEF2A mutations may account for up to 1.93% of the disease population; thus, genetic testing based on mutational analysis of MEF2A may soon be available for many coronary artery disease/myocardial infarction patients. Genome-wide association studies identified significant association for myocardiaI infarction with the LTA gene (encoding lymphotoxin-alpha), and a follow-up study found that an LTA-interacting gene, LGALS2 (encoding galectin-2), is also a susceptibility gene for myocardiaI infarction. Studies that employ genome-wide linkage scans with hundreds of small nuclear families have identified new susceptibility genes for coronary artery disease and myocardiaI infarction, including ALOX5AP (encoding 5-lipoxygenase-activating protein) associated with myocardial infarction and stroke and PDE4D (encoding phosphodiesterase 4D) for ischemic stroke. SUMMARY: Genetic studies provide new insights into the pathogenesis of coronary artery disease and myocardial infarction. Future studies will focus on identification of new disease-causing genes and susceptibility genes, exploration of the molecular mechanisms by which mutations cause coronary artery disease/myocardiaI infarction, and gene-specific therapies for patients.

Indexed as

Molecular Biology3',5'-Cyclic-AMP Phosphodiesterases5-Lipoxygenase-Activating ProteinsCarrier ProteinsCoronary DiseaseCyclic Nucleotide Phosphodiesterases, Type 3Cyclic Nucleotide Phosphodiesterases, Type 4DNA-Binding ProteinsGenetic LinkageGenetic Predisposition to DiseaseHumansLymphotoxin-alphaMADS Domain ProteinsMEF2 Transcription FactorsMembrane ProteinsMutation3',5'-Cyclic-AMP Phosphodiesterases5-Lipoxygenase-Activating ProteinsALOX5AP protein, humanCarrier ProteinsCyclic Nucleotide Phosphodiesterases, Type 3Cyclic Nucleotide Phosphodiesterases, Type 4DNA-Binding ProteinsLymphotoxin-alphaMADS Domain ProteinsMEF2A protein, humanMEF2 Transcription FactorsMembrane ProteinsMyogenic Regulatory FactorsPDE4D protein, humanTranscription Factors

Identifiers

PMID15861005
PMCPMC1579824
OpenAlexW2056451271

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.