Evidence map›Paper›PMID 33195263›Full record

ArticleFrontiers in cell and developmental biology2020

Disease Phenotypes and Mechanisms of iPSC-Derived Cardiomyocytes From Brugada Syndrome Patients With a Loss-of-Function SCN5A Mutation.

Wener Li, Michael Stauske, Xiaojing Luo, Stefan Wagner, Meike Vollrath, Carola S Mehnert, Mario Schubert, Lukas Cyganek, Simin Chen, Sayed-Mohammad Hasheminasab and 5 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.4field-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

24 citing papers in PubMed, 37 citations in OpenAlex.

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  7. High-throughput methods for cardiac cellular electrophysiology studies: the road to personalized medicine.American journal of physiology. Heart and circulatory physiology · 2024
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  12. NovelExperimental and therapeutic medicine · 2023
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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

15 authors at 4 institutions in 1 country.

Wener LiInstitute of Pharmacology and Toxicology, Technische Universität Dresden, Dresden, Germany.
Michael StauskeDepartment of Cardiology and Pneumology, University Medical Center Göttingen, Göttingen, Germany.
Xiaojing LuoInstitute of Pharmacology and Toxicology, Technische Universität Dresden, Dresden, Germany.
Stefan WagnerDepartment of Cardiology and Pneumology, University Medical Center Göttingen, Göttingen, Germany.
Meike VollrathInstitute of Pharmacology and Toxicology, Technische Universität Dresden, Dresden, Germany.
Carola S MehnertInstitute of Pharmacology and Toxicology, Technische Universität Dresden, Dresden, Germany.
Mario SchubertInstitute of Pharmacology and Toxicology, Technische Universität Dresden, Dresden, Germany.
Lukas CyganekDepartment of Cardiology and Pneumology, University Medical Center Göttingen, Göttingen, Germany.
Simin ChenGerman Center for Cardiovascular Research (DZHK), Partner site Göttingen, Göttingen, Germany.
Sayed-Mohammad HasheminasabDepartment of Dermatology, Venereology and Allergy, Charité - Universitätsmedizin Berlin, Berlin, Germany.
Gerald WulfDepartment of Hematology and Oncology, University Medical Center Göttingen, Göttingen, Germany.
Ali El-ArmoucheInstitute of Pharmacology and Toxicology, Technische Universität Dresden, Dresden, Germany.
Lars S MaierDepartment of Cardiology and Pneumology, University Medical Center Göttingen, Göttingen, Germany.
Gerd HasenfussDepartment of Cardiology and Pneumology, University Medical Center Göttingen, Göttingen, Germany.
Kaomei GuanInstitute of Pharmacology and Toxicology, Technische Universität Dresden, Dresden, Germany.
Technische Universität Dresden · DEUniversitätsmedizin Göttingen · DEGerman Centre for Cardiovascular Research · DECharité - Universitätsmedizin Berlin · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Brugada syndrome (BrS) is one of the major causes of sudden cardiac death in young people, while the underlying mechanisms are not completely understood. Here, we investigated the pathophysiological phenotypes and mechanisms using induced pluripotent stem cell (iPSC)-derived cardiomyocytes (CMs) from two BrS patients (BrS-CMs) carrying a heterozygous

Indexed as

Brugada syndromedepolarizationdisease modelinginduced pluripotent stem cellsrepolarizationSCN5A mutation

Identifiers

PMID33195263
PMCPMC7642519
OpenAlexW3083015148

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.