Evidence map›Paper›PMID 26811054›Full record

ArticlePhysiological reports2016

Altered physiological functions and ion currents in atrial fibroblasts from patients with chronic atrial fibrillation.

Claire Poulet, Stephan Künzel, Edgar Büttner, Diana Lindner, Dirk Westermann, Ursula Ravens

Open access · goldAbstract read
In one paragraph

Article in Physiological reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

36 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
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  9. CaBiomolecules · 2024
    Review
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  11. Review
  12. Nonmyocytes as electrophysiological contributors to cardiac excitation and conduction.American journal of physiology. Heart and circulatory physiology · 2023
    Review
  13. Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023
    Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Increased fibroblast accumulation in the equine heart following persistent atrial fibrillation.International journal of cardiology. Heart & vasculature · 2021
    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

6 authors at 3 institutions in 1 country.

Claire PouletDepartment of Pharmacology and Toxicology, Medical Faculty Carl-Gustav-Carus, TU Dresden, Dresden, Germany c.poulet@imperial.ac.uk.
Stephan KünzelDepartment of Pharmacology and Toxicology, Medical Faculty Carl-Gustav-Carus, TU Dresden, Dresden, Germany.
Edgar BüttnerDepartment of Pharmacology and Toxicology, Medical Faculty Carl-Gustav-Carus, TU Dresden, Dresden, Germany.
Diana LindnerDepartment of General and Interventional Cardiology, University Heart Center Hamburg Eppendorf, Hamburg, Germany.
Dirk WestermannDepartment of General and Interventional Cardiology, University Heart Center Hamburg Eppendorf, Hamburg, Germany.
Ursula RavensDepartment of Pharmacology and Toxicology, Medical Faculty Carl-Gustav-Carus, TU Dresden, Dresden, Germany.
TU Dresden · DEUniversity Medical Center Hamburg-Eppendorf · DEUniversity Hospital Carl Gustav Carus · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The contribution of human atrial fibroblasts to cardiac physiology and pathophysiology is poorly understood. Fibroblasts may contribute to arrhythmogenesis through fibrosis, or by directly altering electrical activity in cardiomyocytes. The objective of our study was to uncover phenotypic differences between cells from patients in sinus rhythm (SR) and chronic atrial fibrillation (AF), with special emphasis on electrophysiological properties. We isolated fibroblasts from human right atrial tissue for patch-clamp experiments, proliferation, migration, and differentiation assays, and gene expression profiling. In culture, proliferation and migration of AF fibroblasts were strongly impaired but differentiation into myofibroblasts was increased. This was associated with a higher number of AF fibroblasts expressing functional Nav1.5 channels. Strikingly Na(+) currents were considerably larger in AF cells. Blocking Na(+) channels in culture with tetrodotoxin did not affect proliferation, migration, or differentiation in neither SR nor AF cells. While freshly isolated fibroblasts showed mostly weak rectifier currents, fibroblasts in culture developed outward rectifier K(+) currents of similar amplitude between the SR and AF groups. Adding the K(+) channel blockers tetraethylammonium and 4-aminopyridin in culture reduced current amplitude and inhibited proliferation in the SR group only. Analysis of gene expression revealed significant differences between SR and AF in genes encoding for ion channels, collagen, growth factors, connexins, and cadherins. In conclusion, this study shows that under AF conditions atrial fibroblasts undergo phenotypic changes that are revealed in culture. Future experiments should be performed in situ to understand the nature of those changes and whether they affect cardiac electrical activity.

Indexed as

AgedAtrial FibrillationCell DifferentiationCell MovementCell ProliferationCells, CulturedChronic DiseaseFemaleFibroblastsHeart AtriaHumansImmunohistochemistryIon ChannelsMaleMiddle AgedOligonucleotide Array Sequence AnalysisIon ChannelsAtrial fibrillationelectrophysiologyfibroblasts

Identifiers

PMID26811054
PMCPMC4760386
OpenAlexW2259283850

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.