Evidence map›Paper›PMID 23863953›Full record

ArticleCirculation. Cardiovascular genetics2013

Weighted gene coexpression network analysis of human left atrial tissue identifies gene modules associated with atrial fibrillation.

Nicholas Tan, Mina K Chung, Jonathan D Smith, Jeffrey Hsu, David Serre, David W Newton, Laurie Castel, Edward Soltesz, Gosta Pettersson, A Marc Gillinov and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Circulation. Cardiovascular genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

30 citing papers in PubMed, 46 citations in OpenAlex.

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  12. Distinct peripheral blood monocyte and neutrophil transcriptional programs following intracerebral hemorrhage and different etiologies of ischemic stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021
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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

12 authors at 1 institution in 1 country.

Nicholas TanCleveland Clinic Lerner College of Medicine, Cleveland, OH 44195, USA. tann@ccf.org
Mina K Chung
Jonathan D Smith
Jeffrey Hsu
David Serre
David W Newton
Laurie Castel
Edward Soltesz
Gosta Pettersson
A Marc Gillinov
David R Van Wagoner
John Barnard
Cleveland Clinic Lerner College of Medicine · US

Funding

Functional Genomics of Atrial Fibrillation in Human AtriaR01HL111314 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI BARNARD, JOHN, CHUNG, MINA KAY · 2012 to 2019
$6.1M
Genetics of Atrial FibrillationR01HL090620 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI BARNARD, JOHN, CHUNG, MINA KAY · 2008 to 2012
$2.9M
Molecular Medicine Training ProgramT32GM088088 · NIGMS · CLEVELAND CLINIC LERNER COM-CWRU · PI SMITH, JONATHAN D · 2011 to 2020
$1.7M
NHLBI NIH HHS HL090620NHLBI NIH HHS HL111314NHLBI NIH HHS R01 HL090620NHLBI NIH HHS R01 HL111314NIGMS NIH HHS T32 GM088088
6 · The paper itself

Abstract

backgroundGenetic mechanisms of atrial fibrillation (AF) remain incompletely understood. Previous differential expression studies in AF were limited by small sample size and provided limited understanding of global gene networks, prompting the need for larger-scale, network-based analyses. METHODS AND

resultsLeft atrial tissues from Cleveland Clinic patients who underwent cardiac surgery were assayed using Illumina Human HT-12 mRNA microarrays. The data set included 3 groups based on cardiovascular comorbidities: mitral valve (MV) disease without coronary artery disease (n=64), coronary artery disease without MV disease (n=57), and lone AF (n=35). Weighted gene coexpression network analysis was performed in the MV group to detect modules of correlated genes. Module preservation was assessed in the other 2 groups. Module eigengenes were regressed on AF severity or atrial rhythm at surgery. Modules whose eigengenes correlated with either AF phenotype were analyzed for gene content. A total of 14 modules were detected in the MV group; all were preserved in the other 2 groups. One module (124 genes) was associated with AF severity and atrial rhythm across all groups. Its top hub gene, RCAN1, is implicated in calcineurin-dependent signaling and cardiac hypertrophy. Another module (679 genes) was associated with atrial rhythm in the MV and coronary artery disease groups. It was enriched with cell signaling genes and contained cardiovascular developmental genes including TBX5.

conclusionsOur network-based approach found 2 modules strongly associated with AF. Further analysis of these modules may yield insight into AF pathogenesis by providing novel targets for functional studies.

Indexed as

Gene Regulatory NetworksAgedAtrial FibrillationCalcineurinCluster AnalysisCoronary Artery DiseaseDNA-Binding ProteinsFemaleHeart AtriaHeart Valve DiseasesHumansIntracellular Signaling Peptides and ProteinsMaleMiddle AgedMitral ValveMuscle ProteinsCalcineurinDNA-Binding ProteinsIntracellular Signaling Peptides and ProteinsMuscle ProteinsRCAN1 protein, humanT-Box Domain ProteinsT-box transcription factor 5arrhythmias, cardiacatrial fibrillationbioinformaticsgene coexpressiongene regulatory networksgeneticsmicroarrays

Identifiers

PMID23863953
PMCPMC3955718
OpenAlexW2136565115

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.