Evidence map›Paper›PMID 32383994›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2020

Reduced Na

Janine Ebner, Pavel Uhrin, Petra L Szabo, Attila Kiss, Bruno K Podesser, Hannes Todt, Karlheinz Hilber, Xaver Koenig

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2020. 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
0.5field-weighted citation impact, top 39% 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, 14 citations in OpenAlex.

  1. Review
  2. Article
  3. The sodium/glucose cotransporter 2 inhibitor empagliflozin is a pharmacological chaperone of cardiac NaAmerican journal of physiology. Heart and circulatory physiology · 2025
    Article
  4. Article
  5. Review
  6. Conduction defects and arrhythmias inFrontiers in physiology · 2025
    Article
  7. Article
  8. Empagliflozin treatment rescues abnormally reduced NaAmerican journal of physiology. Heart and circulatory physiology · 2024
    Article
  9. Article
  10. Article
  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

8 authors at 1 institution in 1 country.

Janine EbnerDepartment of Neurophysiology-Pharmacology, Center for Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.ORCID 0000-0002-4180-203X
Pavel UhrinDepartment of Vascular Biology and Thrombosis Research, Center for Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.ORCID 0000-0002-9792-3420
Petra L SzaboLudwig Boltzmann Institute for Cardiovascular Research at the Center for Biomedical Research, Medical University of Vienna, Vienna, Austria.ORCID 0000-0001-5465-8391
Attila KissLudwig Boltzmann Institute for Cardiovascular Research at the Center for Biomedical Research, Medical University of Vienna, Vienna, Austria.
Bruno K PodesserLudwig Boltzmann Institute for Cardiovascular Research at the Center for Biomedical Research, Medical University of Vienna, Vienna, Austria.
Hannes TodtDepartment of Neurophysiology-Pharmacology, Center for Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.ORCID 0000-0002-1147-4370
Karlheinz HilberDepartment of Neurophysiology-Pharmacology, Center for Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.ORCID 0000-0002-3033-0874
Xaver KoenigDepartment of Neurophysiology-Pharmacology, Center for Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.ORCID 0000-0002-2423-4966
Medical University of Vienna · AT

Funding

Austrian Science Fund FWF P 30234
6 · The paper itself

Abstract

Cardiac arrhythmias significantly contribute to mortality in Duchenne muscular dystrophy (DMD), a degenerative muscle disease triggered by mutations in the gene encoding for the intracellular protein dystrophin. A major source for the arrhythmias in patients with DMD is impaired ventricular impulse conduction, which predisposes for ventricular asynchrony, decreased cardiac output, and the development of reentrant mechanisms. The reason for ventricular conduction impairments and the associated arrhythmias in the dystrophic heart has remained unidentified. In the present study, we explored the hypothesis that dystrophin-deficient cardiac Purkinje fibers have reduced Na

Indexed as

Action PotentialsAnimalsArrhythmias, CardiacCardiac Conduction System DiseaseMaleMiceMice, Inbred mdxMuscular Dystrophy, DuchennePurkinje FibersSodiumSodium ChannelsSodiumSodium ChannelsarrhythmiasDuchenne muscular dystrophyNa+ currentPurkinje fibersventricular conduction

Identifiers

PMID32383994
PMCPMC7618121
OpenAlexW3023673985

What OpenQuestion holds

Textmetadata
LicenceTDM
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.