Evidence map›Paper›PMID 35955883›Full record

ReviewInternational journal of molecular sciences2022

Arrhythmogenic Cardiomyopathy: Exercise Pitfalls, Role of Connexin-43, and Moving beyond Antiarrhythmics.

Isabella Leite Coscarella, Maicon Landim-Vieira, José Renato Pinto, Stephen P Chelko

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.6field-weighted citation impact, top 15% 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

11 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. A perspective on Notch signalling in progression and arrhythmogenesis in familial hypertrophic and dilated cardiomyopathies.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023
    Review
  10. Review
  11. Article
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

4 authors at 1 institution in 1 country.

Isabella Leite CoscarellaDepartment of Biomedical Sciences, Florida State University College of Medicine, Tallahassee, FL 32303, USA.ORCID 0000-0001-9706-9319
Maicon Landim-VieiraDepartment of Biomedical Sciences, Florida State University College of Medicine, Tallahassee, FL 32303, USA.ORCID 0000-0002-6696-8888
José Renato PintoDepartment of Biomedical Sciences, Florida State University College of Medicine, Tallahassee, FL 32303, USA.
Stephen P ChelkoDepartment of Biomedical Sciences, Florida State University College of Medicine, Tallahassee, FL 32303, USA.ORCID 0000-0003-1675-5945
Florida State University · US

Funding

American Heart Association 19CDA34760185American Heart Association 2021AHAPRE216237
6 · The paper itself

Abstract

Arrhythmogenic Cardiomyopathy (ACM), a Mendelian disorder that can affect both left and right ventricles, is most often associated with pathogenic desmosomal variants that can lead to fibrofatty replacement of the myocardium, a pathological hallmark of this disease. Current therapies are aimed to prevent the worsening of disease phenotypes and sudden cardiac death (SCD). Despite the use of implantable cardioverter defibrillators (ICDs) there is no present therapy that would mitigate the loss in electrical signal and propagation by these fibrofatty barriers. Recent studies have shown the influence of forced vs. voluntary exercise in a variety of healthy and diseased mice; more specifically, that exercised mice show increased Connexin-43 (Cx43) expression levels. Fascinatingly, increased Cx43 expression ameliorated the abnormal electrical signal conduction in the myocardium of diseased mice. These findings point to a major translational pitfall in current therapeutics for ACM patients, who are advised to completely cease exercising and already demonstrate reduced Cx43 levels at the myocyte intercalated disc. Considering cardiac dysfunction in ACM arises from the loss of cardiomyocytes and electrical signal conduction abnormalities, an increase in Cx43 expression-promoted by low to moderate intensity exercise and/or gene therapy-could very well improve cardiac function in ACM patients.

Indexed as

Arrhythmogenic Right Ventricular DysplasiaAnimalsAnti-Arrhythmia AgentsCardiac Conduction System DiseaseConnexin 43Death, Sudden, CardiacHeart VentriclesMiceMyocardiumAnti-Arrhythmia AgentsConnexin 43arrhythmogenic cardiomyopathyconnexin-43exercisefibrofatty infiltration

Identifiers

PMID35955883
PMCPMC9369094
OpenAlexW4290516270

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.