Evidence map›Paper›PMID 38266112›Full record

ReviewArteriosclerosis, thrombosis, and vascular biology2024

Genome-Wide Genetic Associations Prioritize Evaluation of Causal Mechanisms of Atherosclerotic Disease Risk.

Thomas Quertermous, Daniel Yuhang Li, Chad S Weldy, Markus Ramste, Disha Sharma, João P Monteiro, Wenduo Gu, Matthew D Worssam, Brian T Palmisano, Chong Y Park and 1 more

Abstract readReview
In one paragraph

Review in Arteriosclerosis, thrombosis, and vascular biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. 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

11 authors.

Thomas QuertermousDivision of Cardiovascular Medicine, Stanford University School of Medicine, CA.ORCID 0000-0002-7645-9067
Daniel Yuhang LiDivision of Cardiovascular Medicine, Stanford University School of Medicine, CA.ORCID 0000-0003-1015-6298
Chad S WeldyDivision of Cardiovascular Medicine, Stanford University School of Medicine, CA.ORCID 0000-0003-4652-6422
Markus RamsteDivision of Cardiovascular Medicine, Stanford University School of Medicine, CA.ORCID 0000-0003-4048-4591
Disha SharmaDivision of Cardiovascular Medicine, Stanford University School of Medicine, CA.ORCID 0000-0001-9486-2709
João P MonteiroDivision of Cardiovascular Medicine, Stanford University School of Medicine, CA.
Wenduo GuDivision of Cardiovascular Medicine, Stanford University School of Medicine, CA.ORCID 0000-0002-3859-3150
Matthew D WorssamDivision of Cardiovascular Medicine, Stanford University School of Medicine, CA.ORCID 0000-0003-4391-5377
Brian T PalmisanoDivision of Cardiovascular Medicine, Stanford University School of Medicine, CA.ORCID 0000-0002-2140-1060
Chong Y ParkDivision of Cardiovascular Medicine, Stanford University School of Medicine, CA.
Paul ChengDivision of Cardiovascular Medicine, Stanford University School of Medicine, CA.ORCID 0000-0003-3429-2702

Funding

Stanford Mendelian Genomics Research CenterU01HG011762 · NHGRI · STANFORD UNIVERSITY · PI Jonathan Adam Bernstein, Stephen Montgomery · 2021 to 2026
$16.7M
Stanford Center for Connecting DNA Variants to Function and PhenotypeUM1HG011972 · NHGRI · STANFORD UNIVERSITY · PI JESSE M ENGREITZ, THOMAS QUERTERMOUS · 2021 to 2026
$10.5M
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
The SMAD3 signaling network in coronary artery disease riskR01HL139478 · NHLBI · STANFORD UNIVERSITY · PI THOMAS QUERTERMOUS · 2018 to 2026
$3.7M
PDGFD regulates a transcriptional network to modulate smooth muscle cell transition and coronary artery disease riskR01HL156846 · NHLBI · STANFORD UNIVERSITY · PI QUERTERMOUS, THOMAS · 2021 to 2024
$2.7M
Identifying tobacco-genetic interactions through study of the aryl hydrocarbon receptor pathway.R01HL151535 · NHLBI · STANFORD UNIVERSITY · PI QUERTERMOUS, THOMAS · 2021 to 2024
$2.7M
Molecular mechanisms of vascular calcification and their connection to coronary disease riskR01HL158525 · NHLBI · STANFORD UNIVERSITY · PI QUERTERMOUS, THOMAS · 2022 to 2025
$2.4M
Gene regulatory networks controlling smooth muscle phenotype and vasculardisease riskR01HL171045 · NHLBI · STANFORD UNIVERSITY · PI THOMAS QUERTERMOUS · 2024 to 2026
$2.1M
LncRNA Transcriptional Mechanisms of Coronary Artery Disease RiskR01HL145708 · NHLBI · STANFORD UNIVERSITY · PI QUERTERMOUS, THOMAS · 2019 to 2022
$1.6M
Identification of causal coronary heart disease variation in smooth muscle cellsR33HL120757 · NHLBI · STANFORD UNIVERSITY · PI QUERTERMOUS, THOMAS · 2016 to 2018
$1.6M
American Heart Association-American Stroke Association 23CDA1042900American Heart Association-American Stroke Association 23POST1018991NHGRI NIH HHS U01 HG011762NHGRI NIH HHS UM1 HG011972NHLBI NIH HHS F32 HL165819NHLBI NIH HHS F32 HL165854NHLBI NIH HHS K08 HL153798NHLBI NIH HHS K08 HL167699NHLBI NIH HHS R01 HL109512NHLBI NIH HHS R01 HL134817NHLBI NIH HHS R01 HL139478NHLBI NIH HHS R01 HL145708NHLBI NIH HHS R01 HL151535NHLBI NIH HHS R01 HL156846NHLBI NIH HHS R01 HL158525NHLBI NIH HHS R01 HL171045NHLBI NIH HHS R21 HL120757NHLBI NIH HHS R33 HL120757NHLBI NIH HHS T32 HL098049
6 · The paper itself

Abstract

objectiveThe goal of this review is to discuss the implementation of genome-wide association studies to identify causal mechanisms of vascular disease risk. APPROACH AND

resultsThe history of genome-wide association studies is described, the use of imputation and the creation of consortia to conduct meta-analyses with sufficient power to arrive at consistent associated loci for vascular disease. Genomic methods are described that allow the identification of causal variants and causal genes and how they impact the disease process. The power of single-cell analyses to promote genome-wide association studies of causal gene function is described.

conclusionsGenome-wide association studies represent a paradigm shift in the study of cardiovascular disease, providing identification of genes, cellular phenotypes, and disease pathways that empower the future of targeted drug development.

Indexed as

Cardiovascular DiseasesVascular DiseasesDrug DevelopmentGenome-Wide Association StudyGenomicsHumanscardiovascular diseasesdisease susceptibilitygenomicsphenotypevascular diseases

Identifiers

PMID38266112
PMCPMC10857784

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.