Evidence map›Paper›PMID 24065831›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2013

Shear stress triggers insertion of voltage-gated potassium channels from intracellular compartments in atrial myocytes.

Hannah E Boycott, Camille S M Barbier, Catherine A Eichel, Kevin D Costa, Raphael P Martins, Florent Louault, Gilles Dilanian, Alain Coulombe, Stéphane N Hatem, Elise Balse

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 2 pooled it
2.8field-weighted citation impact, top 9% 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

43 citing papers in PubMed, 2 syntheses or guidelines pooled it, 84 citations in OpenAlex.

  1. Pooled it
  2. Guideline
  3. Evidence for a role of adverse sarcomere signaling in atrial fibrillation induction.Journal of molecular and cellular cardiology plus · 2026
    Review
  4. Article
  5. Observational
  6. mScience China. Life sciences · 2025
    Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. KInternational journal of molecular sciences · 2021
    Article
  19. Review
  20. 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

10 authors at 3 institutions in 2 countries.

Hannah E BoycottLIA/Transatlantic Cardiovascular Research Center, Université Pierre et Marie Curie, 75005 Paris, France and Mount Sinai School of Medicine, New York, NY 10029-6574.
Camille S M Barbier
Catherine A Eichel
Kevin D Costa
Raphael P Martins
Florent Louault
Gilles Dilanian
Alain Coulombe
Stéphane N Hatem
Elise Balse
Icahn School of Medicine at Mount Sinai · USInserm · FRSorbonne Université · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atrial myocytes are continuously exposed to mechanical forces including shear stress. However, in atrial myocytes, the effects of shear stress are poorly understood, particularly with respect to its effect on ion channel function. Here, we report that shear stress activated a large outward current from rat atrial myocytes, with a parallel decrease in action potential duration. The main ion channel underlying the increase in current was found to be Kv1.5, the recruitment of which could be directly observed by total internal reflection fluorescence microscopy, in response to shear stress. The effect was primarily attributable to recruitment of intracellular pools of Kv1.5 to the sarcolemma, as the response was prevented by the SNARE protein inhibitor N-ethylmaleimide and the calcium chelator BAPTA. The process required integrin signaling through focal adhesion kinase and relied on an intact microtubule system. Furthermore, in a rat model of chronic hemodynamic overload, myocytes showed an increase in basal current despite a decrease in Kv1.5 protein expression, with a reduced response to shear stress. Additionally, integrin beta1d expression and focal adhesion kinase activation were increased in this model. This data suggests that, under conditions of chronically increased mechanical stress, the integrin signaling pathway is overactivated, leading to increased functional Kv1.5 at the membrane and reducing the capacity of cells to further respond to mechanical challenge. Thus, pools of Kv1.5 may comprise an inducible reservoir that can facilitate the repolarization of the atrium under conditions of excessive mechanical stress.

Indexed as

Analysis of VarianceAnimalsBiomechanical PhenomenaBlotting, WesternEgtazic AcidEthylmaleimideFluorescent Antibody TechniqueHeart AtriaIntegrin beta1Kv1.5 Potassium ChannelMaleMicroscopy, FluorescenceModels, BiologicalMyocytes, CardiacPatch-Clamp TechniquesRats1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acidEgtazic AcidEthylmaleimideIntegrin beta1Kv1.5 Potassium ChannelSNARE Proteinscardiomyocytespotassium currenttrafficking

Identifiers

PMID24065831
PMCPMC3799377
OpenAlexW2168522301

What OpenQuestion holds

Textmetadata
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.