Evidence map›Paper›PMID 31043074›Full record

ReviewArteriosclerosis, thrombosis, and vascular biology2019

Genetic Insights Into Smooth Muscle Cell Contributions to Coronary Artery Disease.

Doris Wong, Adam W Turner, Clint L Miller

Open access · bronzeAbstract readReview
In one paragraph

Review in Arteriosclerosis, thrombosis, and vascular biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 2 pooled it
3.8field-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

22 citing papers in PubMed, 2 syntheses or guidelines pooled it, 39 citations in OpenAlex.

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  16. Journal of clinical medicine · 2022
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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

3 authors at 2 institutions in 1 country.

Doris WongFrom the Center for Public Health Genomics (D.W., A.W.T., C.L.M.), University of Virginia, Charlottesville.
Adam W TurnerFrom the Center for Public Health Genomics (D.W., A.W.T., C.L.M.), University of Virginia, Charlottesville.
Clint L MillerFrom the Center for Public Health Genomics (D.W., A.W.T., C.L.M.), University of Virginia, Charlottesville.
University of Virginia · USVirginia Department of Health · US

Funding

Multimodal genetic regulatory architecture of coronary artery diseaseR01HL148239 · NHLBI · UNIVERSITY OF VIRGINIA · PI Clint L Miller · 2019 to 2026
$4.2M
EPISTATIC REGULATORY MECHANISMS OF CORONARY HEART DISEASE RISKR00HL125912 · NHLBI · UNIVERSITY OF VIRGINIA · PI MILLER, CLINT L · 2017 to 2019
$747k
Epistatic Regulatory Mechanisms of Coronary Heart Disease RiskK99HL125912 · NHLBI · STANFORD UNIVERSITY · PI MILLER, CLINT L · 2015 to 2016
$285k
NHLBI NIH HHS K99 HL125912NHLBI NIH HHS R00 HL125912NHLBI NIH HHS R01 HL148239
6 · The paper itself

Abstract

Coronary artery disease is a complex cardiovascular disease involving an interplay of genetic and environmental influences over a lifetime. Although considerable progress has been made in understanding lifestyle risk factors, genetic factors identified from genome-wide association studies may capture additional hidden risk undetected by traditional clinical tests. These genetic discoveries have highlighted many candidate genes and pathways dysregulated in the vessel wall, including those involving smooth muscle cell phenotypic modulation and injury responses. Here, we summarize experimental evidence for a few genome-wide significant loci supporting their roles in smooth muscle cell biology and disease. We also discuss molecular quantitative trait locus mapping as a powerful discovery and fine-mapping approach applied to smooth muscle cell and coronary artery disease-relevant tissues. We emphasize the critical need for alternative genetic strategies, including cis/trans-regulatory network analysis, genome editing, and perturbations, as well as single-cell sequencing in smooth muscle cell tissues and model organisms, under both normal and disease states. By integrating multiple experimental and analytical modalities, these multidimensional datasets should improve the interpretation of coronary artery disease genome-wide association studies and molecular quantitative trait locus signals and inform candidate targets for therapeutic intervention or risk prediction.

Indexed as

Genetic Predisposition to DiseaseGenome-Wide Association StudyCoronary Artery DiseaseCoronary VesselsHumansLife StyleMuscle, Smooth, VascularMyocytes, Smooth MusclePhenotypePolymorphism, Single NucleotideQuantitative Trait LociRisk AssessmentSensitivity and Specificitycoronary artery diseasegene editinggenome-wide association studyquantitative trait locirisk factorsvascular smooth muscle cells

Identifiers

PMID31043074
PMCPMC8909916
OpenAlexW2943532730

What OpenQuestion holds

Textmetadata
LicenceTDM
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.