Evidence map›Paper›PMID 29940860›Full record

ArticleBMC genomics2018

The arrhythmogenic cardiomyopathy-specific coding and non-coding transcriptome in human cardiac stromal cells.

Johannes Rainer, Viviana Meraviglia, Hagen Blankenburg, Chiara Piubelli, Peter P Pramstaller, Adolfo Paolin, Elisa Cogliati, Giulio Pompilio, Elena Sommariva, Francisco S Domingues and 1 more

Open access · goldAbstract read
In one paragraph

Article in BMC genomics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 11% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

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  20. LncRNA TUG1 contributes to cardiac hypertrophy via regulating miR-29b-3p.In vitro cellular & developmental biology. Animal · 2019
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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 3 institutions in 1 country.

Johannes RainerInstitute for Biomedicine, Eurac Research, Affiliated Institute of the University of Lübeck, Viale Druso 1, 39100, Bolzano, Italy. johannes.rainer@eurac.edu.ORCID http://orcid.org/0000-0002-6977-7147
Viviana MeravigliaInstitute for Biomedicine, Eurac Research, Affiliated Institute of the University of Lübeck, Viale Druso 1, 39100, Bolzano, Italy. viviana.meraviglia@eurac.edu.
Hagen BlankenburgInstitute for Biomedicine, Eurac Research, Affiliated Institute of the University of Lübeck, Viale Druso 1, 39100, Bolzano, Italy.
Chiara PiubelliInstitute for Biomedicine, Eurac Research, Affiliated Institute of the University of Lübeck, Viale Druso 1, 39100, Bolzano, Italy.
Peter P PramstallerInstitute for Biomedicine, Eurac Research, Affiliated Institute of the University of Lübeck, Viale Druso 1, 39100, Bolzano, Italy.
Adolfo PaolinTreviso Tissue Bank Foundation, Piazzalo Ospedale 1, 31100, Treviso, Italy.
Elisa CogliatiTreviso Tissue Bank Foundation, Piazzalo Ospedale 1, 31100, Treviso, Italy.
Giulio PompilioVascular Biology and Regenerative Medicine Unit, Centro Cardiologico Monzino IRCCS, via Parea 4, 20138, Milan, Italy.
Elena SommarivaVascular Biology and Regenerative Medicine Unit, Centro Cardiologico Monzino IRCCS, via Parea 4, 20138, Milan, Italy.
Francisco S DominguesInstitute for Biomedicine, Eurac Research, Affiliated Institute of the University of Lübeck, Viale Druso 1, 39100, Bolzano, Italy.
Alessandra RossiniInstitute for Biomedicine, Eurac Research, Affiliated Institute of the University of Lübeck, Viale Druso 1, 39100, Bolzano, Italy.
Eurac Research · ITCentro Cardiologico Monzino · ITVeneto Eye Bank Foundation · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundArrhythmogenic cardiomyopathy (ACM) is a genetic autosomal disease characterized by abnormal cell-cell adhesion, cardiomyocyte death, progressive fibro-adipose replacement of the myocardium, arrhythmias and sudden death. Several different cell types contribute to the pathogenesis of ACM, including, as recently described, cardiac stromal cells (CStCs). In the present study, we aim to identify ACM-specific expression profiles of human CStCs derived from endomyocardial biopsies of ACM patients and healthy individuals employing TaqMan Low Density Arrays for miRNA expression profiling, and high throughput sequencing for gene expression quantification.

resultsWe identified 3 miRNAs and 272 genes as significantly differentially expressed at a 5% false discovery rate. Both the differentially expressed genes as well as the target genes of the ACM-specific miRNAs were found to be enriched in cell adhesion-related biological processes. Functional similarity and protein interaction-based network analyses performed on the identified deregulated genes, miRNA targets and known ACM-causative genes revealed clusters of highly related genes involved in cell adhesion, extracellular matrix organization, lipid transport and ephrin receptor signaling.

conclusionsWe determined for the first time the coding and non-coding transcriptome characteristic of ACM cardiac stromal cells, finding evidence for a potential contribution of miRNAs, specifically miR-29b-3p, to ACM pathogenesis or phenotype maintenance.

Indexed as

Arrhythmias, CardiacCardiomyopathiesGene Expression ProfilingGenomicsHumansMicroRNAsTranscriptomeMicroRNAsArrhythmogenic cardiomyopathyCardiac stromal cellsGene expressionGenomicsmicroRNA expressionTranscriptome profiling

Identifiers

PMID29940860
PMCPMC6019788
OpenAlexW2810977809

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Registered trials

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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.