Evidence map›Paper›PMID 39120296›Full record

ReviewCells2024

In Vivo Approaches to Understand Arrhythmogenic Cardiomyopathy: Perspectives on Animal Models.

Giovanni Risato, Raquel Brañas Casas, Marco Cason, Maria Bueno Marinas, Serena Pinci, Monica De Gaspari, Silvia Visentin, Stefania Rizzo, Gaetano Thiene, Cristina Basso and 3 more

Abstract readReview
In one paragraph

Review in Cells, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Review
  2. Review
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

13 authors.

Giovanni RisatoDepartment of Cardio-Thoraco-Vascular Sciences and Public Health, University of Padua, I-35128 Padua, Italy.ORCID 0000-0003-0651-7409
Raquel Brañas CasasDepartment of Biology, University of Padua, I-35131 Padua, Italy.ORCID 0000-0002-0908-4330
Marco CasonDepartment of Cardio-Thoraco-Vascular Sciences and Public Health, University of Padua, I-35128 Padua, Italy.ORCID 0000-0003-3051-8065
Maria Bueno MarinasDepartment of Cardio-Thoraco-Vascular Sciences and Public Health, University of Padua, I-35128 Padua, Italy.ORCID 0000-0001-9601-3671
Serena PinciDepartment of Cardio-Thoraco-Vascular Sciences and Public Health, University of Padua, I-35128 Padua, Italy.
Monica De GaspariDepartment of Cardio-Thoraco-Vascular Sciences and Public Health, University of Padua, I-35128 Padua, Italy.
Silvia VisentinDepartment of Women's and Children's Health, University of Padua, I-35128 Padua, Italy.
Stefania RizzoDepartment of Cardio-Thoraco-Vascular Sciences and Public Health, University of Padua, I-35128 Padua, Italy.ORCID 0000-0001-5969-4412
Gaetano ThieneDepartment of Cardio-Thoraco-Vascular Sciences and Public Health, University of Padua, I-35128 Padua, Italy.ORCID 0000-0002-8814-2577
Cristina BassoDepartment of Cardio-Thoraco-Vascular Sciences and Public Health, University of Padua, I-35128 Padua, Italy.ORCID 0000-0002-0195-9753
Kalliopi PilichouDepartment of Cardio-Thoraco-Vascular Sciences and Public Health, University of Padua, I-35128 Padua, Italy.ORCID 0000-0003-3646-0669
Natascia TisoDepartment of Biology, University of Padua, I-35131 Padua, Italy.ORCID 0000-0002-5444-9853
Rudy CeleghinDepartment of Cardio-Thoraco-Vascular Sciences and Public Health, University of Padua, I-35128 Padua, Italy.ORCID 0000-0001-9047-9032

Funding

Italian Ministry of Health RF-2019-12370183Italian Ministry of University and Research PNRR M4C2 CN00000041Italian Ministry of University and Research PRIN 20173ZWACSItalian Ministry of University and Research PRIN 20229FE439Italian Ministry of University and Research PRIN 2022WZCXRZItalian Telethon Foundation GGP19287PNRR Next-Generation EU PNRR-MR1-2022-12376614Veneto Region Target Research 933/2015
6 · The paper itself

Abstract

Arrhythmogenic cardiomyopathy (AC) is a hereditary cardiac disorder characterized by the gradual replacement of cardiomyocytes with fibrous and adipose tissue, leading to ventricular wall thinning, chamber dilation, arrhythmias, and sudden cardiac death. Despite advances in treatment, disease management remains challenging. Animal models, particularly mice and zebrafish, have become invaluable tools for understanding AC's pathophysiology and testing potential therapies. Mice models, although useful for scientific research, cannot fully replicate the complexity of the human AC. However, they have provided valuable insights into gene involvement, signalling pathways, and disease progression. Zebrafish offer a promising alternative to mammalian models, despite the phylogenetic distance, due to their economic and genetic advantages. By combining animal models with in vitro studies, researchers can comprehensively understand AC, paving the way for more effective treatments and interventions for patients and improving their quality of life and prognosis.

Indexed as

Disease Models, AnimalAnimalsArrhythmias, CardiacArrhythmogenic Right Ventricular DysplasiaCardiomyopathiesHumansMiceZebrafishanimal modelsarrhythmogenic cardiomyopathyheartmousezebrafish

Identifiers

PMID39120296
PMCPMC11311808

What OpenQuestion holds

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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.