Evidence map›Paper›PMID 23617620›Full record

ArticleJournal of cellular and molecular medicine2013

Cyclical stretch induces structural changes in atrial myocytes.

Anne Margreet De Jong, Alexander H Maass, Silke U Oberdorf-Maass, Rudolf A De Boer, Wiek H Van Gilst, Isabelle C Van Gelder

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

22 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
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  3. Review
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  8. Impact of low-voltage zones on the left atrial anterior wall on the reduction in the left atrial appendage flow velocity in persistent atrial fibrillation patients.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2019
    Article
  9. Cardiac Tissue Chips (CTCs) for Modeling Cardiovascular Disease.IEEE transactions on bio-medical engineering · 2019
    Article
  10. Review
  11. Article
  12. Article
  13. Serine/Threonine Phosphatases in Atrial Fibrillation.Journal of molecular and cellular cardiology · 2017
    Review
  14. Article
  15. Article
  16. p38 MAPK in cardioprotection - are we there yet?British journal of pharmacology · 2015
    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

6 authors at 3 institutions in 1 country.

Anne Margreet De JongDepartment of Cardiology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.
Alexander H Maass
Silke U Oberdorf-Maass
Rudolf A De Boer
Wiek H Van Gilst
Isabelle C Van Gelder
University of Groningen · NLUniversity Medical Center Groningen · NLNetherlands Heart Institute · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atrial fibrillation (AF) often occurs in the presence of an underlying disease. These underlying diseases cause atrial remodelling, which make the atria more susceptible to AF. Stretch is an important mediator in the remodelling process. The aim of this study was to develop an atrial cell culture model mimicking remodelling due to atrial pressure overload. Neonatal rat atrial cardiomyocytes (NRAM) were cultured and subjected to cyclical stretch on elastic membranes. Stretching with 1 Hz and 15% elongation for 30 min. resulted in increased expression of immediate early genes and phosphorylation of Erk and p38. A 24-hr stretch period resulted in hypertrophy-related changes including increased cell diameter, reinduction of the foetal gene program and cell death. No evidence of apoptosis was observed. Expression of atrial natriuretic peptide, brain natriuretic peptide and growth differentiation factor-15 was increased, and calcineurin signalling was activated. Expression of several potassium channels was decreased, suggesting electrical remodelling. Atrial stretch-induced change in skeletal α-actin expression was inhibited by pravastatin, but not by eplerenone or losartan. Stretch of NRAM results in elevation of stress markers, changes related to hypertrophy and dedifferentiation, electrical remodelling and cell death. This model can contribute to investigating the mechanisms involved in the remodelling process caused by stretch and to the testing of pharmaceutical agents.

Indexed as

Atrial RemodelingActinsAnimalsAnimals, NewbornAnticholesteremic AgentsAtrial FibrillationAtrial Natriuretic FactorCalcineurinCell DeathExtracellular Signal-Regulated MAP KinasesGene Expression Regulation, DevelopmentalGrowth Differentiation Factor 15Heart AtriaMyocytes, CardiacNatriuretic Peptide, Brainp38 Mitogen-Activated Protein KinasesActinsAnticholesteremic AgentsAtrial Natriuretic FactorCalcineurinExtracellular Signal-Regulated MAP KinasesGdf15 protein, ratGrowth Differentiation Factor 15Natriuretic Peptide, Brainp38 Mitogen-Activated Protein KinasesPotassium ChannelsPravastatin

Identifiers

PMID23617620
PMCPMC3823178
OpenAlexW2074136431

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.