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

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 g...

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Published inScientific reports Vol. 10; no. 1; p. 10486
Main Authors Shadrina, Alexandra S., Shashkova, Tatiana I., Torgasheva, Anna A., Sharapov, Sodbo Z., Klarić, Lucija, Pakhomov, Eugene D., Alexeev, Dmitry G., Wilson, James F., Tsepilov, Yakov A., Joshi, Peter K., Aulchenko, Yurii S.
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 26.06.2020
Nature Publishing Group
Subjects
631/208/2489/144
692/699/75/593/15
Cardiovascular disease
Computer Simulation
Coronary artery
Coronary Artery Disease - genetics
Coronary vessels
Etiology
Gene expression
Gene loci
Genetic Predisposition to Disease - genetics
Genome-wide association studies
Genome-Wide Association Study - methods
Genomes
Genomics - methods
Heart diseases
Humanities and Social Sciences
Humans
multidisciplinary
Polymorphism, Single Nucleotide - genetics
Quantitative Trait Loci - genetics
Risk Factors
Science
Science (multidisciplinary)
Online AccessGet full text

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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.
AbstractList 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.
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.
ArticleNumber 10486
Author Torgasheva, Anna A.
Shadrina, Alexandra S.
Pakhomov, Eugene D.
Alexeev, Dmitry G.
Joshi, Peter K.
Aulchenko, Yurii S.
Tsepilov, Yakov A.
Sharapov, Sodbo Z.
Klarić, Lucija
Shashkova, Tatiana I.
Wilson, James F.
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Snippet Genome-wide association studies have led to a significant progress in identification of genomic loci affecting coronary artery disease (CAD) risk. However,...
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SubjectTerms 631/208/2489/144
692/699/75/593/15
Cardiovascular disease
Computer Simulation
Coronary artery
Coronary Artery Disease - genetics
Coronary vessels
Etiology
Gene expression
Gene loci
Genetic Predisposition to Disease - genetics
Genome-wide association studies
Genome-Wide Association Study - methods
Genomes
Genomics - methods
Heart diseases
Humanities and Social Sciences
Humans
multidisciplinary
Polymorphism, Single Nucleotide - genetics
Quantitative Trait Loci - genetics
Risk Factors
Science
Science (multidisciplinary)
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Title Prioritization of causal genes for coronary artery disease based on cumulative evidence from experimental and in silico studies
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https://www.ncbi.nlm.nih.gov/pubmed/32591598
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Volume 10
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