Evidence map›Paper›PMID 23557754›Full record

ReviewJournal of molecular and cellular cardiology2013

Channelopathies from mutations in the cardiac sodium channel protein complex.

Graham S Adsit, Ravi Vaidyanathan, Carla M Galler, John W Kyle, Jonathan C Makielski

Open access · greenAbstract readReview
In one paragraph

Review in Journal of molecular and cellular cardiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

26 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Protein 14-3-3 Influences the Response of the Cardiac Sodium Channel NaThe Journal of pharmacology and experimental therapeutics · 2023
    Article
  3. NaStructure (London, England : 1993) · 2021
    Article
  4. Article
  5. Review
  6. Article
  7. Mechanisms of death in structurally normal stillbirths.Journal of perinatal medicine · 2019
    Observational
  8. Computational models in cardiology.Nature reviews. Cardiology · 2019
    Review
  9. Article
  10. Small-conductance CaExperimental & molecular medicine · 2018
    Review
  11. Article
  12. Article
  13. Azithromycin Causes a Novel Proarrhythmic Syndrome.Circulation. Arrhythmia and electrophysiology · 2017
    Article
  14. Review
  15. Review
  16. Voltage-Gated Na+ Channels: Not Just for Conduction.Cold Spring Harbor perspectives in biology · 2016
    Review
  17. Article
  18. Article
  19. Article
  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

5 authors at 2 institutions in 1 country.

Graham S AdsitDepartment of Medicine, Division of Cardiovascular Medicine, University of Wisconsin, Madison, WI 53792, USA.
Ravi Vaidyanathan
Carla M Galler
John W Kyle
Jonathan C Makielski
University of Wisconsin–Madison · USMadison Area Technical College · US

Funding

Training Program in Translational Cardiovascular Science (TPTCS)T32HL007936 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI Lee Lochbaum Eckhardt, Gail A Robertson · 2001 to 2026
$11.6M
Cellular &Clinical Phenotypes of Novel SCN5a MutationsR01HL071092 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI MAKIELSKI, JONATHAN C · 2003 to 2011
$3.1M
The cardiac Na current macromolecular complex and role in arrhythmia mechanismR56HL071092 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI MAKIELSKI, JONATHAN C · 2014 to 2014
$376k
NHLBI NIH HHS HL71092NHLBI NIH HHS R01 HL071092NHLBI NIH HHS R56 HL071092NHLBI NIH HHS T32 HL007936NHLBI NIH HHS T32HL07936
6 · The paper itself

Abstract

The cardiac sodium current underlies excitability in heart, and inherited abnormalities of the proteins regulating and conducting this current cause inherited arrhythmia syndromes. This review focuses on inherited mutations in non-pore forming proteins of sodium channel complexes that cause cardiac arrhythmia, and the deduced mechanisms by which they affect function and dysfunction of the cardiac sodium current. Defining the structure and function of these complexes and how they are regulated will contribute to understanding the possible roles for this complex in normal and abnormal physiology and homeostasis. This article is part of a Special Issue entitled "Na(+) Regulation in Cardiac Myocytes".

Indexed as

Mutation, MissenseAnimalsArrhythmias, CardiacCalcium-Binding ProteinsChannelopathiesHomeostasisHumansMembrane ProteinsMultiprotein ComplexesMuscle ProteinsMyocardial ContractionNAV1.5 Voltage-Gated Sodium ChannelProtein SubunitsCalcium-Binding ProteinsMembrane ProteinsMultiprotein ComplexesMuscle ProteinsNAV1.5 Voltage-Gated Sodium ChannelProtein SubunitsSCN5A protein, humansyntrophin alpha1ArrhythmiaBrugada SyndromeLong QT syndromeSCN5ASIDSSodium current

Identifiers

PMID23557754
PMCPMC3720718
OpenAlexW2013886538

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.