Evidence map›Paper›PMID 37731079›Full record

ReviewStem cell reviews and reports2023

Arrhythmogenic Cardiomyopathy: from Preclinical Models to Genotype-phenotype Correlation and Pathophysiology.

Xuehui Fan, Guoqiang Yang, Firat Duru, Maurizio Grilli, Ibrahim Akin, Xiaobo Zhou, Ardan Muammer Saguner, Ibrahim Ei-Battrawy

Open access · hybridAbstract readReview
In one paragraph

Review in Stem cell reviews and reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
3.3field-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

9 citing papers in PubMed, 15 citations in OpenAlex.

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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

8 authors at 2 institutions in 4 countries.

Xuehui Fan *Key Laboratory of Medical Electrophysiology, Ministry of Education and Medical Electrophysiological Key Laboratory of Sichuan Province, Collaborative Innovation Center for Prevention of Cardiovascular Diseases, Institute of Cardiovascular Research, Southwest Medical University, Luzhou, Sichuan, China.ORCID 0000-0001-9040-1155
Guoqiang Yang *Cardiology, Angiology, Haemostaseology, and Medical Intensive Care, Medical Centre Mannheim, Medical Faculty Mannheim, Heidelberg University, Heidelberg, Germany.
Firat DuruDepartment of Cardiology, University Heart Centre, University Hospital Zurich, Zurich, Switzerland.
Maurizio GrilliFaculty of Medicine, University Medical Centre Mannheim (UMM), University of Heidelberg, Mannheim, Germany.
Ibrahim AkinCardiology, Angiology, Haemostaseology, and Medical Intensive Care, Medical Centre Mannheim, Medical Faculty Mannheim, Heidelberg University, Heidelberg, Germany.
Xiaobo ZhouKey Laboratory of Medical Electrophysiology, Ministry of Education and Medical Electrophysiological Key Laboratory of Sichuan Province, Collaborative Innovation Center for Prevention of Cardiovascular Diseases, Institute of Cardiovascular Research, Southwest Medical University, Luzhou, Sichuan, China. xiaobo.zhou@medma.uni-heidelberg.de.
Ardan Muammer Saguner *Department of Cardiology, University Heart Centre, University Hospital Zurich, Zurich, Switzerland.
Ibrahim Ei-Battrawy *European Center for AngioScience (ECAS), German Center for Cardiovascular Research (DZHK) Partner Site Heidelberg/ Mannheim, and Centre for Cardiovascular Acute Medicine Mannheim (ZKAM), Medical Centre Mannheim, Heidelberg University, Partner Site, Heidelberg-Mannheim, Germany. Ibrahim.elbattrawy2006@gmail.com.
Heidelberg University · DEUniversity Hospital of Zurich · CH

Funding

Foundation of the Education Department of Sichuan Province 17ZB0476National Nature Science Foundation of China 82200361Natural Science Foundation of Sichuan Province 22NSFSC3053Southwest Medical University Scientific Research Fund 2021ZKMS035the Foundation of Office of Science & Technology of Luzhou City 2021-JYJ-70
6 · The paper itself

Abstract

Arrhythmogenic cardiomyopathy (ACM) is a hereditary myocardial disease characterized by the replacement of the ventricular myocardium with fibrous fatty deposits. ACM is usually inherited in an autosomal dominant pattern with variable penetrance and expressivity, which is mainly related to ventricular tachyarrhythmia and sudden cardiac death (SCD). Importantly, significant progress has been made in determining the genetic background of ACM due to the development of new techniques for genetic analysis. The exact molecular pathomechanism of ACM, however, is not completely clear and the genotype-phenotype correlations have not been fully elucidated, which are useful to predict the prognosis and treatment of ACM patients. Different gene-targeted and transgenic animal models, human-induced pluripotent stem cell-derived cardiomyocyte (hiPSC-CM) models, and heterologous expression systems have been developed. Here, this review aims to summarize preclinical ACM models and platforms promoting our understanding of the pathogenesis of ACM and assess their value in elucidating the ACM genotype-phenotype relationship.

Indexed as

Heart VentriclesInduced Pluripotent Stem CellsAnimalsHumansMyocardiumMyocytes, CardiacAnimal modelsArrhythmogenic cardiomyopathyDesmosomesHuman-induced pluripotent stem cell-derived cardiomyocytesPathophysiology

Identifiers

PMID37731079
PMCPMC10661732
OpenAlexW4386883020

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.