Evidence map›Paper›PMID 27586139›Full record

ReviewCurrent cardiology reports2016

Genetics and Genomics of Coronary Artery Disease.

Milos Pjanic, Clint L Miller, Robert Wirka, Juyong B Kim, Daniel M DiRenzo, Thomas Quertermous

Abstract readReview
In one paragraph

Review in Current cardiology reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–field-weighted citation impact
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

19 citing papers in PubMed.

  1. A comprehensive review of m6 A methylation in coronary heart disease.Journal of molecular medicine (Berlin, Germany) · 2025
    Review
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  13. Association of theInternational journal of clinical and experimental pathology · 2018
    Article
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  15. Observational
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  17. Review
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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

6 authors.

Milos PjanicDepartment of Medicine, Division of Cardiovascular Medicine, Cardiovascular Institute, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, CA, 94305-5233, USA.
Clint L MillerDepartment of Medicine, Division of Cardiovascular Medicine, Cardiovascular Institute, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, CA, 94305-5233, USA.
Robert WirkaDepartment of Medicine, Division of Cardiovascular Medicine, Cardiovascular Institute, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, CA, 94305-5233, USA.
Juyong B KimDepartment of Medicine, Division of Cardiovascular Medicine, Cardiovascular Institute, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, CA, 94305-5233, USA.
Daniel M DiRenzoDepartment of Medicine, Division of Cardiovascular Medicine, Cardiovascular Institute, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, CA, 94305-5233, USA.
Thomas QuertermousDepartment of Medicine, Division of Cardiovascular Medicine, Cardiovascular Institute, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, CA, 94305-5233, USA. tomq1@stanford.edu.

Funding

Identifying the gene networks of insulin resistance: the GENESIPS studyU01HL107388 · NHLBI · STANFORD UNIVERSITY · PI QUERTERMOUS, THOMAS, SCHADT, ERIC E · 2011 to 2015
$8.8M
T32 Training Program in Mechanisms and Innovation in Vascular DiseaseT32HL098049 · NHLBI · STANFORD UNIVERSITY · PI Nicholas James Leeper, Philip S Tsao · 2010 to 2026
$6.3M
Causal variant association mechanisms in TCF21 binding coronary disease lociR01HL134817 · NHLBI · STANFORD UNIVERSITY · PI THOMAS QUERTERMOUS · 2017 to 2026
$6.2M
Mechanism of the Coronary Heart Disease Association at Chromosome 6q23.2R01HL109512 · NHLBI · STANFORD UNIVERSITY · PI QUERTERMOUS, THOMAS · 2011 to 2019
$6.1M
Training in Myocardial Biology at Stanford (TIMBS)T32HL094274 · NHLBI · STANFORD UNIVERSITY · PI Euan A Ashley, Daniel Bernstein · 2010 to 2026
$5.0M
Regulation of Inflammation and Atherosclerosis by TCF21K08HL133375 · NHLBI · STANFORD UNIVERSITY · PI KIM, JUYONG BRIAN · 2016 to 2020
$840k
EPISTATIC REGULATORY MECHANISMS OF CORONARY HEART DISEASE RISKR00HL125912 · NHLBI · UNIVERSITY OF VIRGINIA · PI MILLER, CLINT L · 2017 to 2019
$747k
Identification of causal coronary heart disease variation in smooth muscle cellsR21HL120757 · NHLBI · STANFORD UNIVERSITY · PI QUERTERMOUS, THOMAS · 2014 to 2015
$434k
Epistatic Regulatory Mechanisms of Coronary Heart Disease RiskK99HL125912 · NHLBI · STANFORD UNIVERSITY · PI MILLER, CLINT L · 2015 to 2016
$285k
The role of TCF21 in coronary heart diseaseF32HL129670 · NHLBI · STANFORD UNIVERSITY · PI WIRKA, ROBERT · 2015 to 2017
$192k
NHLBI NIH HHS F32 HL129670NHLBI NIH HHS K08 HL133375NHLBI NIH HHS K99 HL125912NHLBI NIH HHS R00 HL125912NHLBI NIH HHS R01 HL109512NHLBI NIH HHS R01 HL134817NHLBI NIH HHS R21 HL120757NHLBI NIH HHS T32 HL094274NHLBI NIH HHS T32 HL098049NHLBI NIH HHS U01 HL107388
6 · The paper itself

Abstract

Coronary artery disease (or coronary heart disease), is the leading cause of mortality in many of the developing as well as the developed countries of the world. Cholesterol-enriched plaques in the heart's blood vessels combined with inflammation lead to the lesion expansion, narrowing of blood vessels, reduced blood flow, and may subsequently cause lesion rupture and a heart attack. Even though several environmental risk factors have been established, such as high LDL-cholesterol, diabetes, and high blood pressure, the underlying genetic composition may substantially modify the disease risk; hence, genome composition and gene-environment interactions may be critical for disease progression. Ongoing scientific efforts have seen substantial advancements related to the fields of genetics and genomics, with the major breakthroughs yet to come. As genomics is the most rapidly advancing field in the life sciences, it is important to present a comprehensive overview of current efforts. Here, we present a summary of various genetic and genomics assays and approaches applied to coronary artery disease research.

Indexed as

GenomicsAnimalsCoronary Artery DiseaseCRISPR-Cas SystemsDisease Models, AnimalDisease ProgressionGene DeletionGene-Environment InteractionGenetic Predisposition to DiseaseHumansMolecular Targeted TherapyRisk FactorsCoronary artery diseaseEpigeneticsGeneticsGenomicsGWASTranscriptomics

Identifiers

PMID27586139
PMCPMC5872834

What OpenQuestion holds

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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.