Evidence map›Paper›PMID 33802229›Full record

ReviewInternational journal of molecular sciences2021

iPSC-Cardiomyocyte Models of Brugada Syndrome-Achievements, Challenges and Future Perspectives.

Aleksandra Nijak, Johan Saenen, Alain J Labro, Dorien Schepers, Bart L Loeys, Maaike Alaerts

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

19 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
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  8. Role of NF-κB signaling pathway in HIn vitro cellular & developmental biology. Animal · 2024
    Article
  9. Zebrafish as a Model System for Brugada Syndrome.Reviews in cardiovascular medicine · 2024
    Review
  10. Identification of a novelFrontiers in cardiovascular medicine · 2024
    Article
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  12. Review
  13. Article
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  15. Article
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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

6 authors at 2 institutions in 2 countries.

Aleksandra NijakCenter of Medical Genetics, Faculty of Medicine and Health Sciences, University of Antwerp and Antwerp University Hospital, 2650 Antwerp, Belgium.
Johan SaenenDepartment of Cardiology, Faculty of Medicine and Health Sciences, University of Antwerp and Antwerp University Hospital, 2610 Antwerp, Belgium.
Alain J LabroDepartment of Biomedical Sciences, Faculty of Pharmaceutical, Biomedical and Veterinary Sciences, University of Antwerp, 2610 Antwerp, Belgium.
Dorien SchepersCenter of Medical Genetics, Faculty of Medicine and Health Sciences, University of Antwerp and Antwerp University Hospital, 2650 Antwerp, Belgium.ORCID 0000-0003-4225-6621
Bart L LoeysCenter of Medical Genetics, Faculty of Medicine and Health Sciences, University of Antwerp and Antwerp University Hospital, 2650 Antwerp, Belgium.ORCID 0000-0003-3703-9518
Maaike AlaertsCenter of Medical Genetics, Faculty of Medicine and Health Sciences, University of Antwerp and Antwerp University Hospital, 2650 Antwerp, Belgium.ORCID 0000-0002-1376-3635
University of Antwerp · BERadboud University Nijmegen · NL

Funding

European Research Council ERC-COG-2017-771945Fonds Wetenschappelijk Onderzoek G.0356.17; 1S24317NUniversiteit Antwerpen GOA
6 · The paper itself

Abstract

Brugada syndrome (BrS) is an inherited cardiac arrhythmia that predisposes to ventricular fibrillation and sudden cardiac death. It originates from oligogenic alterations that affect cardiac ion channels or their accessory proteins. The main hurdle for the study of the functional effects of those variants is the need for a specific model that mimics the complex environment of human cardiomyocytes. Traditionally, animal models or transient heterologous expression systems are applied for electrophysiological investigations, each of these models having their limitations. The ability to create induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs), providing a source of human patient-specific cells, offers new opportunities in the field of cardiac disease modelling. Contemporary iPSC-CMs constitute the best possible in vitro model to study complex cardiac arrhythmia syndromes such as BrS. To date, thirteen reports on iPSC-CM models for BrS have been published and with this review we provide an overview of the current findings, with a focus on the electrophysiological parameters. We also discuss the methods that are used for cell derivation and data acquisition. In the end, we critically evaluate the knowledge gained by the use of these iPSC-CM models and discuss challenges and future perspectives for iPSC-CMs in the study of BrS and other arrhythmias.

Indexed as

Models, CardiovascularBrugada SyndromeHumansInduced Pluripotent Stem CellsMyocytes, Cardiacbrugada syndromeelectrophysiologyinduced pluripotent stem cellsinherited cardiac arrhythmiaiPSC-cardiomyocytes

Identifiers

PMID33802229
PMCPMC8001521
OpenAlexW3135856967

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.