Evidence map›Paper›PMID 27122098›Full record

ArticleNature communications2016

Myoscape controls cardiac calcium cycling and contractility via regulation of L-type calcium channel surface expression.

Matthias Eden, Benjamin Meder, Mirko Völkers, Montatip Poomvanicha, Katrin Domes, M Branchereau, P Marck, Rainer Will, Alexander Bernt, Ashraf Rangrez and 8 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

15 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Presynaptic L-Type CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  10. Article
  11. Review
  12. Article
  13. Augmentation of myocardial INature communications · 2019
    Article
  14. STRIP1, a core component of STRIPAK complexes, is essential for normal mesoderm migration in the mouse embryo.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  15. STRIP2 Is Indispensable for the Onset of Embryonic Stem Cell Differentiation.Molecular therapy. Methods & clinical development · 2017
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

18 authors at 7 institutions in 2 countries.

Matthias EdenDepartment of Internal Medicine III (Cardiology and Angiology), University Hospital Schleswig-Holstein, Campus Kiel, 24105 Kiel, Germany.
Benjamin MederDepartment of Internal Medicine III, University of Heidelberg, 69120 Heidelberg, Germany.
Mirko VölkersDepartment of Internal Medicine III, University of Heidelberg, 69120 Heidelberg, Germany.
Montatip PoomvanichaDepartment of Pharmacology, University of Technology Munich, 80333 Munich, Germany.
Katrin DomesDepartment of Pharmacology, University of Technology Munich, 80333 Munich, Germany.
M BranchereauInserm U1048 - Institut des Maladies Métaboliques et Cardiovasculaires (I2MC)/Equipe 13, Bat L4 1er étage C.H.U Rangueil 1 av Jean Poulhès - BP 84225 31432 Toulouse Cedex 4, France.
P MarckInserm U1048 - Institut des Maladies Métaboliques et Cardiovasculaires (I2MC)/Equipe 13, Bat L4 1er étage C.H.U Rangueil 1 av Jean Poulhès - BP 84225 31432 Toulouse Cedex 4, France.
Rainer WillDepartment of Internal Medicine III, University of Heidelberg, 69120 Heidelberg, Germany.
Alexander BerntGerman Centre for Cardiovascular Research, partner site 20246 Hamburg/24105 Kiel/23562 Lübeck, Germany.
Ashraf RangrezGerman Centre for Cardiovascular Research, partner site 20246 Hamburg/24105 Kiel/23562 Lübeck, Germany.
Matthias BuschDepartment of Internal Medicine III, University of Heidelberg, 69120 Heidelberg, Germany.
German Mouse Clinic Consortium
Martin Hrabě de AngelisGerman Mouse Clinic, Institute of Experimental Genetics, Helmholtz Zentrum München, German Research Center for Environmental Health, 85764 Neuherberg, Germany.
Christophe HeymesInserm U1048 - Institut des Maladies Métaboliques et Cardiovasculaires (I2MC)/Equipe 13, Bat L4 1er étage C.H.U Rangueil 1 av Jean Poulhès - BP 84225 31432 Toulouse Cedex 4, France.
Wolfgang RottbauerDepartment of Internal Medicine III, Cardiology and Angiology, University Hospital of Ulm, 89081 Ulm, Germany.
Patrick MostDepartment of Internal Medicine III, University of Heidelberg, 69120 Heidelberg, Germany.
Franz HofmannDepartment of Pharmacology, University of Technology Munich, 80333 Munich, Germany.
Norbert FreyDepartment of Internal Medicine III (Cardiology and Angiology), University Hospital Schleswig-Holstein, Campus Kiel, 24105 Kiel, Germany.
Heidelberg University · DEInserm · FRMunich University of Applied Sciences · DEGerman Centre for Cardiovascular Research · DEUniversity Hospital Schleswig-Holstein · DEHelmholtz Zentrum München · DEUniversity Hospital Ulm · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Calcium signalling plays a critical role in the pathogenesis of heart failure. Here we describe a cardiac protein named Myoscape/FAM40B/STRIP2, which directly interacts with the L-type calcium channel. Knockdown of Myoscape in cardiomyocytes decreases calcium transients associated with smaller Ca(2+) amplitudes and a lower diastolic Ca(2+) content. Likewise, L-type calcium channel currents are significantly diminished on Myoscape ablation, and downregulation of Myoscape significantly reduces contractility of cardiomyocytes. Conversely, overexpression of Myoscape increases global Ca(2+) transients and enhances L-type Ca(2+) channel currents, and is sufficient to restore decreased currents in failing cardiomyocytes. In vivo, both Myoscape-depleted morphant zebrafish and Myoscape knockout (KO) mice display impairment of cardiac function progressing to advanced heart failure. Mechanistically, Myoscape-deficient mice show reduced L-type Ca(2+)currents, cell capacity and calcium current densities as a result of diminished LTCC surface expression. Finally, Myoscape expression is reduced in hearts from patients suffering of terminal heart failure, implying a role in human disease.

Indexed as

Gene Expression RegulationAnimalsAnimals, NewbornCalciumCalcium Channels, L-TypeCarrier ProteinsCells, CulturedCytoskeletal ProteinsHEK293 CellsHumansMice, Inbred C57BLMice, KnockoutMyocardial ContractionMyocardiumMyocytes, CardiacProtein BindingCACNA1C protein, humanCalciumCalcium Channels, L-TypeCarrier ProteinsCytoskeletal ProteinsSTRIP2 protein, human

Identifiers

PMID27122098
PMCPMC5438100
OpenAlexW2342555258

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.