Evidence map›Paper›PMID 32348453›Full record

ReviewCardiovascular research2020

Genetic basis and molecular biology of cardiac arrhythmias in cardiomyopathies.

Ali J Marian, Babken Asatryan, Xander H T Wehrens

Abstract readReview
In one paragraph

Review in Cardiovascular research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing 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

35 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Role of CaArchives of toxicology · 2023
    Review
  16. Online Databases of Genome Editing in Cardiovascular and Metabolic Diseases.Advances in experimental medicine and biology · 2023
    Article
  17. Review
  18. Article
  19. Review
  20. 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

3 authors.

Ali J MarianDepartment of Medicine, Center for Cardiovascular Genetics, Institute of Molecular Medicine, University of Texas Health Sciences Center at Houston, 6770 Bertner Street, Suite C900A, Houston, TX 77030, USA.
Babken AsatryanDepartment of Cardiology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland.
Xander H T WehrensDepartment of Biophysics and Molecular Physiology, Cardiovascular Research Institute, Baylor College of Medicine, Houston, TX 77030, USA.

Funding

Pathogenic Role of Selected Cardiac Myocyte- and Fibroblast-Specific Epigenetic Changes in LaminopathiesR01HL132401 · NHLBI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI Ali J Marian · 2016 to 2026
$6.0M
Cell type-Specific Therapeutic Targeting of canonical WNT Pathway in Arrhythmogenic CardiomyopathyR01HL151737 · NHLBI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI MARIAN, ALI J · 2020 to 2023
$2.0M
Cardiovascular Ultrasonography UnitS10OD018135 · OD · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI MARIAN, ALI J · 2015 to 2015
$184k
NHLBI NIH HHS R01 HL132401NHLBI NIH HHS R01 HL151737NIH HHS S10 OD018135
6 · The paper itself

Abstract

Cardiac arrhythmias are common, often the first, and sometimes the life-threatening manifestations of hereditary cardiomyopathies. Pathogenic variants in several genes known to cause hereditary cardiac arrhythmias have also been identified in the sporadic cases and small families with cardiomyopathies. These findings suggest a shared genetic aetiology of a subset of hereditary cardiomyopathies and cardiac arrhythmias. The concept of a shared genetic aetiology is in accord with the complex and exquisite interplays that exist between the ion currents and cardiac mechanical function. However, neither the causal role of cardiac arrhythmias genes in cardiomyopathies is well established nor the causal role of cardiomyopathy genes in arrhythmias. On the contrary, secondary changes in ion currents, such as post-translational modifications, are common and contributors to the pathogenesis of arrhythmias in cardiomyopathies through altering biophysical and functional properties of the ion channels. Moreover, structural changes, such as cardiac hypertrophy, dilatation, and fibrosis provide a pro-arrhythmic substrate in hereditary cardiomyopathies. Genetic basis and molecular biology of cardiac arrhythmias in hereditary cardiomyopathies are discussed.

Indexed as

MutationAction PotentialsAnimalsAnti-Arrhythmia AgentsArrhythmias, CardiacCardiomyopathiesCatheter AblationDeath, Sudden, CardiacGenetic Predisposition to DiseaseHeart RateHeredityHumansPhenotypePrognosisRisk AssessmentRisk FactorsAnti-Arrhythmia AgentsGenetics • Cardiomyopathy • Arrhythmias • Ion channels • Electrophysiology • Sudden death

Identifiers

PMID32348453
PMCPMC7341170

What OpenQuestion holds

Textmetadata
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.