Evidence map›Paper›PMID 37438479›Full record

ArticleScientific reports2023

Cytoskeletal disarray increases arrhythmogenic vulnerability during sympathetic stimulation in a model of hypertrophic cardiomyopathy.

Henrietta Cserne Szappanos, Helena M Viola, Danica W Ito, Seakcheng Lim, Melissa Mangala, Mira Holliday, Samantha Barratt Ross, Christopher Semsarian, Adam Hill, Rose E Dixon and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Atrial electrophysiology in hypertrophic cardiomyopathy: current insights and knowledge gaps.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2026
    Review
  2. Review
  3. Early Cytoskeletal Remodeling Drives Hypertrophic Cardiomyopathy Pathogenesis inJournal of cardiovascular development and disease · 2025
    Article
  4. 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

11 authors at 5 institutions in 2 countries.

Henrietta Cserne SzappanosSchool of Human Sciences, University of Western Australia, Crawley, WA, Australia.
Helena M ViolaSchool of Human Sciences, University of Western Australia, Crawley, WA, Australia.
Danica W ItoDepartment of Physiology and Membrane Biology, University of California, Davis, CA, USA.
Seakcheng LimAgnes Ginges Centre for Molecular Cardiology, Centenary Institute, Sydney, Australia.
Melissa MangalaVictor Chang Cardiac Research Institute, Sydney, NSW, Australia.
Mira HollidayAgnes Ginges Centre for Molecular Cardiology, Centenary Institute, Sydney, Australia.
Samantha Barratt RossAgnes Ginges Centre for Molecular Cardiology, Centenary Institute, Sydney, Australia.
Christopher SemsarianAgnes Ginges Centre for Molecular Cardiology, Centenary Institute, Sydney, Australia.
Adam HillVictor Chang Cardiac Research Institute, Sydney, NSW, Australia.
Rose E DixonDepartment of Physiology and Membrane Biology, University of California, Davis, CA, USA.
Livia C HoolSchool of Human Sciences, University of Western Australia, Crawley, WA, Australia. livia.hool@uwa.edu.au.
University of Sydney · AUUniversity of Western Australia · AUUniversity of California, Davis · USVictor Chang Cardiac Research Institute · AUCentenary Institute · AU

Funding

Training Program In Basic & Translational Cardiovascular ScienceT32HL086350 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Martin Cadeiras, David A. Liem · 2008 to 2026
$7.1M
Molecular choreography of CaV1.2 channels in the aging myocardiumR01AG063796 · NIA · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Rose Ellen Dixon · 2019 to 2026
$3.1M
American Heart Association-American Stroke Association 15SDG25560035NHLBI NIH HHS T32 HL086350NIA NIH HHS R01 AG063796NIH HHS T32 HL086350
6 · The paper itself

Abstract

Familial hypertrophic cardiomyopathy (FHC) patients are advised to avoid strenuous exercise due to increased risk of arrhythmias. Mice expressing the human FHC-causing mutation R403Q in the myosin heavy chain gene (MYH6) recapitulate the human phenotype, including cytoskeletal disarray and increased arrhythmia susceptibility. Following in vivo administration of isoproterenol, mutant mice exhibited tachyarrhythmias, poor recovery and fatigue. Arrhythmias were attenuated with the β-blocker atenolol and protein kinase A inhibitor PKI. Mutant cardiac myocytes had significantly prolonged action potentials and triggered automaticity due to reduced repolarization reserve and connexin 43 expression. Isoproterenol shortened cycle length, and escalated electrical instability. Surprisingly isoproterenol did not increase Ca

Indexed as

Cardiomyopathy, HypertrophicCardiomyopathy, Hypertrophic, FamilialAnimalsArrhythmias, CardiacHeartHumansIsoproterenolMiceIsoproterenol

Identifiers

PMID37438479
PMCPMC10338442
OpenAlexW4384028961

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.