Evidence map›Paper›PMID 32591598›Full record

SynthesisScientific reports2020

Prioritization of causal genes for coronary artery disease based on cumulative evidence from experimental and in silico studies.

Alexandra S Shadrina, Tatiana I Shashkova, Anna A Torgasheva, Sodbo Z Sharapov, Lucija Klarić, Eugene D Pakhomov, Dmitry G Alexeev, James F Wilson, Yakov A Tsepilov, Peter K Joshi and 1 more

Open access · goldAbstract readMeta-Analysis
In one paragraph

Synthesis in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 4 pooled it
5.0field-weighted citation impact, top 4% 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

26 citing papers in PubMed, 4 syntheses or guidelines pooled it, 41 citations in OpenAlex.

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  7. Improving T2D machine learning-based prediction accuracy with SNPs and younger age.Computational and structural biotechnology journal · 2025
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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

11 authors at 6 institutions in 4 countries.

Alexandra S ShadrinaLaboratory of Theoretical and Applied Functional Genomics, Novosibirsk State University, Novosibirsk, 630090, Russia. weiner.alexserg@gmail.com.
Tatiana I ShashkovaLaboratory of Theoretical and Applied Functional Genomics, Novosibirsk State University, Novosibirsk, 630090, Russia.
Anna A TorgashevaLaboratory of Theoretical and Applied Functional Genomics, Novosibirsk State University, Novosibirsk, 630090, Russia.
Sodbo Z SharapovLaboratory of Theoretical and Applied Functional Genomics, Novosibirsk State University, Novosibirsk, 630090, Russia.
Lucija KlarićGenos Glycoscience Research Laboratory, Zagreb, Croatia.
Eugene D PakhomovLaboratory of Theoretical and Applied Functional Genomics, Novosibirsk State University, Novosibirsk, 630090, Russia.
Dmitry G AlexeevLaboratory of Theoretical and Applied Functional Genomics, Novosibirsk State University, Novosibirsk, 630090, Russia.
James F WilsonMRC Human Genetics Unit, Institute of Genetics and Molecular Medicine, University of Edinburgh, Western General Hospital, Edinburgh, EH4 2XU, Scotland, UK.
Yakov A TsepilovLaboratory of Theoretical and Applied Functional Genomics, Novosibirsk State University, Novosibirsk, 630090, Russia.
Peter K JoshiUsher Institute, University of Edinburgh, Edinburgh, EH8 9AG, Scotland, UK.
Yurii S AulchenkoLaboratory of Recombination and Segregation Analysis, Institute of Cytology and Genetics, Novosibirsk, 630090, Russia. yurii@bionet.nsc.ru.
Novosibirsk State University · RUInstitute of Cytology and Genetics · RUGenos (Croatia) · HRInstitute for Information Transmission Problems · RUInstitute of Genetics and Cancer · GBUniversity of Edinburgh · GB

Funding

Medical Research Council MC_UU_00007/10Medical Research Council MR/R026408/1
6 · The paper itself

Abstract

Genome-wide association studies have led to a significant progress in identification of genomic loci affecting coronary artery disease (CAD) risk. However, revealing the causal genes responsible for the observed associations is challenging. In the present study, we aimed to prioritize CAD-relevant genes based on cumulative evidence from the published studies and our own study of colocalization between eQTLs and loci associated with CAD using SMR/HEIDI approach. Prior knowledge of candidate genes was extracted from both experimental and in silico studies, employing different prioritization algorithms. Our review systematized information for a total of 51 CAD-associated loci. We pinpointed 37 genes in 36 loci. For 27 genes we infer they are causal for CAD, and for 10 further genes we judge them most likely causal. Colocalization analysis showed that for 18 out of these loci, association with CAD can be explained by changes in gene expression in one or more CAD-relevant tissues. Furthermore, for 8 out of 36 loci, existing evidence suggested additional CAD-associated genes. For the remaining 15 loci, we concluded that evidence for gene prioritization remains inconsistent, insufficient, or absent. Our results provide deeper insights into the genetic etiology of CAD and demonstrate knowledge gaps where further research is warranted.

Indexed as

Computer SimulationCoronary Artery DiseaseGenetic Predisposition to DiseaseGenome-Wide Association StudyGenomicsHumansPolymorphism, Single NucleotideQuantitative Trait LociRisk Factors

Identifiers

PMID32591598
PMCPMC7320185
OpenAlexW3037404046

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.