Evidence map›Paper›PMID 24623178›Full record

ReviewCurrent atherosclerosis reports2014

Dissecting the causal genetic mechanisms of coronary heart disease.

Clint L Miller, Themistocles L Assimes, Stephen B Montgomery, Thomas Quertermous

Abstract readReview
In one paragraph

Review in Current atherosclerosis reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Genetics and Genomics of Coronary Artery Disease.Current cardiology reports · 2016
    Review
  9. Article
  10. Cholesterol confusion and statin controversy.World journal of cardiology · 2015
    Review
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.

Clint L MillerDepartment of Medicine, Division of Cardiovascular Medicine, Cardiovascular Institute, Stanford University, 300 Pasteur Drive, Stanford, CA, 94305-5233, USA.
Themistocles L Assimes
Stephen B Montgomery
Thomas Quertermous

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
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
Identification and study of the vascular disease gene at 9p21.3R01HL103635 · NHLBI · STANFORD UNIVERSITY · PI QUERTERMOUS, THOMAS · 2010 to 2013
$2.4M
Identification of causal coronary heart disease variation in smooth muscle cellsR33HL120757 · NHLBI · STANFORD UNIVERSITY · PI QUERTERMOUS, THOMAS · 2016 to 2018
$1.6M
Identification of causal coronary heart disease variation in smooth muscle cellsR21HL120757 · NHLBI · STANFORD UNIVERSITY · PI QUERTERMOUS, THOMAS · 2014 to 2015
$434k
NHLBI NIH HHS R01 HL103635NHLBI NIH HHS R01 HL109512NHLBI NIH HHS R21 HL120757NHLBI NIH HHS R33 HL120757NHLBI NIH HHS T32 HL094274NHLBI NIH HHS U01 HL107388
6 · The paper itself

Abstract

Large-scale genome-wide association studies (GWAS) have identified 46 loci that are associated with coronary heart disease (CHD). Additionally, 104 independent candidate variants (false discovery rate of 5 %) have been identified (Schunkert H, Konig IR, Kathiresan S, Reilly MP, Assimes TL, Holm H et al. Nat Genet 43:333-8, 2011; Deloukas P, Kanoni S, Willenborg C, Farrall M, Assimes TL, Thompson JR et al. Nat Genet 45:25-33, 2012; C4D Genetics Consortium. Nat Genet 43:339-44, 2011). The majority of the causal genes in these loci function independently of conventional risk factors. It is postulated that a number of the CHD-associated genes regulate basic processes in the vascular cells involved in atherosclerosis, and that study of the signaling pathways that are modulated in this cell type by causal regulatory variation will provide critical new insights for targeting the initiation and progression of disease. In this review, we will discuss the types of experimental approaches and data that are critical to understanding the molecular processes that underlie the disease risk at 9p21.3, TCF21, SORT1, and other CHD-associated loci.

Indexed as

Genetic Predisposition to DiseaseAnimalsCoronary DiseaseGenome-Wide Association StudyHumansMutationPolymorphism, Single NucleotideRisk Factors

Identifiers

PMID24623178
PMCPMC4015632

What OpenQuestion holds

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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.