Evidence map›Paper›PMID 27226008›Full record

ArticleCardiovascular research2016

Elevated ventricular wall stress disrupts cardiomyocyte t-tubule structure and calcium homeostasis.

Michael Frisk, Marianne Ruud, Emil K S Espe, Jan Magnus Aronsen, Åsmund T Røe, Lili Zhang, Per Andreas Norseng, Ole M Sejersted, Geir A Christensen, Ivar Sjaastad and 1 more

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In one paragraph

Article in Cardiovascular research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed, 1 pooled it
–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

68 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Cardiac Cell Remodeling in Obesity and Diabetes.Handbook of experimental pharmacology · 2026
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  6. Electrophysiological tolerance: a new concept for understanding the electrical stability of the heart.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2024
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. The interplay of inflammation, exosomes and CaCardiovascular diabetology · 2023
    Review
  14. Article
  15. Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2022
    Article
  16. Serial block face scanning electron microscopy reveals region-dependent remodelling of transverse tubules post-myocardial infarction.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2022
    Article
  17. Article
  18. Article
  19. Review
  20. Article

8 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors.

Michael FriskInstitute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Ullevål, Kirkeveien 166, 0424 Oslo, Norway K.G. Jebsen Cardiac Research Center and Center for Heart Failure Research, University of Oslo, 0316 Oslo, Norway michael.frisk@medisin.uio.no.
Marianne RuudInstitute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Ullevål, Kirkeveien 166, 0424 Oslo, Norway K.G. Jebsen Cardiac Research Center and Center for Heart Failure Research, University of Oslo, 0316 Oslo, Norway.
Emil K S EspeInstitute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Ullevål, Kirkeveien 166, 0424 Oslo, Norway K.G. Jebsen Cardiac Research Center and Center for Heart Failure Research, University of Oslo, 0316 Oslo, Norway.
Jan Magnus AronsenBjørknes College, Oslo, Norway.
Åsmund T RøeInstitute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Ullevål, Kirkeveien 166, 0424 Oslo, Norway K.G. Jebsen Cardiac Research Center and Center for Heart Failure Research, University of Oslo, 0316 Oslo, Norway.
Lili ZhangInstitute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Ullevål, Kirkeveien 166, 0424 Oslo, Norway K.G. Jebsen Cardiac Research Center and Center for Heart Failure Research, University of Oslo, 0316 Oslo, Norway.
Per Andreas NorsengInstitute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Ullevål, Kirkeveien 166, 0424 Oslo, Norway K.G. Jebsen Cardiac Research Center and Center for Heart Failure Research, University of Oslo, 0316 Oslo, Norway.
Ole M SejerstedInstitute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Ullevål, Kirkeveien 166, 0424 Oslo, Norway K.G. Jebsen Cardiac Research Center and Center for Heart Failure Research, University of Oslo, 0316 Oslo, Norway.
Geir A ChristensenInstitute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Ullevål, Kirkeveien 166, 0424 Oslo, Norway K.G. Jebsen Cardiac Research Center and Center for Heart Failure Research, University of Oslo, 0316 Oslo, Norway.
Ivar SjaastadInstitute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Ullevål, Kirkeveien 166, 0424 Oslo, Norway K.G. Jebsen Cardiac Research Center and Center for Heart Failure Research, University of Oslo, 0316 Oslo, Norway.
William E LouchInstitute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Ullevål, Kirkeveien 166, 0424 Oslo, Norway K.G. Jebsen Cardiac Research Center and Center for Heart Failure Research, University of Oslo, 0316 Oslo, Norway.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsInvaginations of the cellular membrane called t-tubules are essential for maintaining efficient excitation-contraction coupling in ventricular cardiomyocytes. Disruption of t-tubule structure during heart failure has been linked to dyssynchronous, slowed Ca(2+) release and reduced power of the heartbeat. The underlying mechanism is, however, unknown. We presently investigated whether elevated ventricular wall stress triggers remodelling of t-tubule structure and function. METHODS AND

resultsMRI and blood pressure measurements were employed to examine regional wall stress across the left ventricle of sham-operated and failing, post-infarction rat hearts. In failing hearts, elevated left ventricular diastolic pressure and ventricular dilation resulted in markedly increased wall stress, particularly in the thin-walled region proximal to the infarct. High wall stress in this proximal zone was associated with reduced expression of the dyadic anchor junctophilin-2 and disrupted cardiomyocyte t-tubular structure. Indeed, local wall stress measurements predicted t-tubule density across sham and failing hearts. Elevated wall stress and disrupted cardiomyocyte structure in the proximal zone were also associated with desynchronized Ca(2+) release in cardiomyocytes and markedly reduced local contractility in vivo. A causative role of wall stress in promoting t-tubule remodelling was established by applying stretch to papillary muscles ex vivo under culture conditions. Loads comparable to wall stress levels observed in vivo in the proximal zone reduced expression of junctophilin-2 and promoted t-tubule loss.

conclusionElevated wall stress reduces junctophilin-2 expression and disrupts t-tubule integrity, Ca(2+) release, and contractile function. These findings provide new insight into the role of wall stress in promoting heart failure progression.

Indexed as

Calcium SignalingMyocardial ContractionVentricular Function, LeftAnimalsBiomechanical PhenomenaCalciumCells, CulturedDisease Models, AnimalDisease ProgressionDown-RegulationExcitation Contraction CouplingHeart FailureHeart VentriclesHomeostasisMaleMembrane ProteinsCalciumjunctophilinMembrane ProteinsCa2+ homeostasisHeart failureJunctophilin-2Left ventricular wall stressT-tubules

Identifiers

PMID27226008
PMCPMC5031949

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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.