Research ExplorerPublicationsTissue-specific multi-omics analysis of atrial fibrillation

Tissue-specific multi-omics analysis of atrial fibrillation

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Tissue-specific multi-omics analysis of atrial fibrillation. / Assum, Ines; Krause, Julia; Scheinhardt, Markus O; Müller, Christian; Hammer, Elke; Börschel, Christin S; Völker, Uwe; Conradi, Lenard; Geelhoed, Bastiaan; Zeller, Tanja; Schnabel, Renate B; Heinig, Matthias.

In: NAT COMMUN, Vol. 13, No. 1, 441, 21.01.2022.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Assum, I, Krause, J, Scheinhardt, MO, Müller, C, Hammer, E, Börschel, CS, Völker, U, Conradi, L, Geelhoed, B, Zeller, T, Schnabel, RB & Heinig, M 2022, 'Tissue-specific multi-omics analysis of atrial fibrillation', NAT COMMUN, vol. 13, no. 1, 441. https://doi.org/10.1038/s41467-022-27953-1

APA

Assum, I., Krause, J., Scheinhardt, M. O., Müller, C., Hammer, E., Börschel, C. S., Völker, U., Conradi, L., Geelhoed, B., Zeller, T., Schnabel, R. B., & Heinig, M. (2022). Tissue-specific multi-omics analysis of atrial fibrillation. NAT COMMUN, 13(1), [441]. https://doi.org/10.1038/s41467-022-27953-1

Vancouver

Assum I, Krause J, Scheinhardt MO, Müller C, Hammer E, Börschel CS et al. Tissue-specific multi-omics analysis of atrial fibrillation. NAT COMMUN. 2022 Jan 21;13(1). 441. https://doi.org/10.1038/s41467-022-27953-1

Bibtex

@article{a5e0f093a6864a7dbec8964870465d23,
title = "Tissue-specific multi-omics analysis of atrial fibrillation",
abstract = "Genome-wide association studies (GWAS) for atrial fibrillation (AF) have uncovered numerous disease-associated variants. Their underlying molecular mechanisms, especially consequences for mRNA and protein expression remain largely elusive. Thus, refined multi-omics approaches are needed for deciphering the underlying molecular networks. Here, we integrate genomics, transcriptomics, and proteomics of human atrial tissue in a cross-sectional study to identify widespread effects of genetic variants on both transcript (cis-eQTL) and protein (cis-pQTL) abundance. We further establish a novel targeted trans-QTL approach based on polygenic risk scores to determine candidates for AF core genes. Using this approach, we identify two trans-eQTLs and five trans-pQTLs for AF GWAS hits, and elucidate the role of the transcription factor NKX2-5 as a link between the GWAS SNP rs9481842 and AF. Altogether, we present an integrative multi-omics method to uncover trans-acting networks in small datasets and provide a rich resource of atrial tissue-specific regulatory variants for transcript and protein levels for cardiovascular disease gene prioritization.",
author = "Ines Assum and Julia Krause and Scheinhardt, {Markus O} and Christian M{\"u}ller and Elke Hammer and B{\"o}rschel, {Christin S} and Uwe V{\"o}lker and Lenard Conradi and Bastiaan Geelhoed and Tanja Zeller and Schnabel, {Renate B} and Matthias Heinig",
note = "{\textcopyright} 2022. The Author(s).",
year = "2022",
month = jan,
day = "21",
doi = "10.1038/s41467-022-27953-1",
language = "English",
volume = "13",
journal = "NAT COMMUN",
issn = "2041-1723",
publisher = "NATURE PUBLISHING GROUP",
number = "1",

}

RIS

TY - JOUR

T1 - Tissue-specific multi-omics analysis of atrial fibrillation

AU - Assum, Ines

AU - Krause, Julia

AU - Scheinhardt, Markus O

AU - Müller, Christian

AU - Hammer, Elke

AU - Börschel, Christin S

AU - Völker, Uwe

AU - Conradi, Lenard

AU - Geelhoed, Bastiaan

AU - Zeller, Tanja

AU - Schnabel, Renate B

AU - Heinig, Matthias

N1 - © 2022. The Author(s).

PY - 2022/1/21

Y1 - 2022/1/21

N2 - Genome-wide association studies (GWAS) for atrial fibrillation (AF) have uncovered numerous disease-associated variants. Their underlying molecular mechanisms, especially consequences for mRNA and protein expression remain largely elusive. Thus, refined multi-omics approaches are needed for deciphering the underlying molecular networks. Here, we integrate genomics, transcriptomics, and proteomics of human atrial tissue in a cross-sectional study to identify widespread effects of genetic variants on both transcript (cis-eQTL) and protein (cis-pQTL) abundance. We further establish a novel targeted trans-QTL approach based on polygenic risk scores to determine candidates for AF core genes. Using this approach, we identify two trans-eQTLs and five trans-pQTLs for AF GWAS hits, and elucidate the role of the transcription factor NKX2-5 as a link between the GWAS SNP rs9481842 and AF. Altogether, we present an integrative multi-omics method to uncover trans-acting networks in small datasets and provide a rich resource of atrial tissue-specific regulatory variants for transcript and protein levels for cardiovascular disease gene prioritization.

AB - Genome-wide association studies (GWAS) for atrial fibrillation (AF) have uncovered numerous disease-associated variants. Their underlying molecular mechanisms, especially consequences for mRNA and protein expression remain largely elusive. Thus, refined multi-omics approaches are needed for deciphering the underlying molecular networks. Here, we integrate genomics, transcriptomics, and proteomics of human atrial tissue in a cross-sectional study to identify widespread effects of genetic variants on both transcript (cis-eQTL) and protein (cis-pQTL) abundance. We further establish a novel targeted trans-QTL approach based on polygenic risk scores to determine candidates for AF core genes. Using this approach, we identify two trans-eQTLs and five trans-pQTLs for AF GWAS hits, and elucidate the role of the transcription factor NKX2-5 as a link between the GWAS SNP rs9481842 and AF. Altogether, we present an integrative multi-omics method to uncover trans-acting networks in small datasets and provide a rich resource of atrial tissue-specific regulatory variants for transcript and protein levels for cardiovascular disease gene prioritization.

U2 - 10.1038/s41467-022-27953-1

DO - 10.1038/s41467-022-27953-1

M3 - SCORING: Journal article

C2 - 35064145

VL - 13

JO - NAT COMMUN

JF - NAT COMMUN

SN - 2041-1723

IS - 1

M1 - 441

ER -