Evidence map›Paper›PMID 25332206›Full record

ArticleCirculation research2014

Dependence of cardiac transverse tubules on the BAR domain protein amphiphysin II (BIN-1).

Jessica L Caldwell, Charlotte E R Smith, Rebecca F Taylor, Ashraf Kitmitto, David A Eisner, Katharine M Dibb, Andrew W Trafford

Open access · greenAbstract read
In one paragraph

Article in Circulation research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed
6.3field-weighted citation impact, top 3% 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

87 citing papers in PubMed, 129 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Cardiac Cell Remodeling in Obesity and Diabetes.Handbook of experimental pharmacology · 2026
    Review
  5. Article
  6. Article
  7. Bend it like BIN1: how a membrane-curving adaptor protein shapes cardiac physiology.American journal of physiology. Heart and circulatory physiology · 2025
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Matriglycan maintains t-tubule structural integrity in cardiac muscle.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Mechanisms of spontaneous CaThe Journal of physiology · 2023
    Article

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

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

7 authors at 1 institution in 1 country.

Jessica L CaldwellFrom the Unit of Cardiac Physiology and Cardiac Biophysics Group, Institute of Cardiovascular Sciences, Manchester Academic Health Science Centre, University of Manchester, Manchester, United Kingdom.
Charlotte E R SmithFrom the Unit of Cardiac Physiology and Cardiac Biophysics Group, Institute of Cardiovascular Sciences, Manchester Academic Health Science Centre, University of Manchester, Manchester, United Kingdom.
Rebecca F TaylorFrom the Unit of Cardiac Physiology and Cardiac Biophysics Group, Institute of Cardiovascular Sciences, Manchester Academic Health Science Centre, University of Manchester, Manchester, United Kingdom.
Ashraf KitmittoFrom the Unit of Cardiac Physiology and Cardiac Biophysics Group, Institute of Cardiovascular Sciences, Manchester Academic Health Science Centre, University of Manchester, Manchester, United Kingdom.
David A EisnerFrom the Unit of Cardiac Physiology and Cardiac Biophysics Group, Institute of Cardiovascular Sciences, Manchester Academic Health Science Centre, University of Manchester, Manchester, United Kingdom.
Katharine M DibbFrom the Unit of Cardiac Physiology and Cardiac Biophysics Group, Institute of Cardiovascular Sciences, Manchester Academic Health Science Centre, University of Manchester, Manchester, United Kingdom.
Andrew W TraffordFrom the Unit of Cardiac Physiology and Cardiac Biophysics Group, Institute of Cardiovascular Sciences, Manchester Academic Health Science Centre, University of Manchester, Manchester, United Kingdom. Andrew.W.Trafford@manchester.ac.uk.
Manchester Academic Health Science Centre · GB

Funding

British Heart Foundation CH/2000/04British Heart Foundation FS/09/002/26487British Heart Foundation FS/09/036/27823British Heart Foundation FS/10/52/28678British Heart Foundation FS/10/71/28563British Heart Foundation FS/12/57/29717British Heart Foundation FS/14/4/30532British Heart Foundation PG/09/062/27872British Heart Foundation PG/10/89/28630British Heart Foundation PG/11/16/28777British Heart Foundation PG/12/89/29970British Heart Foundation RG/11/2/28701Wellcome TrustWellcome Trust 097280
6 · The paper itself

Abstract

rationaleTransverse tubules (t-tubules) regulate cardiac excitation-contraction coupling and exhibit interchamber and interspecies differences in expression. In cardiac disease, t-tubule loss occurs and affects the systolic calcium transient. However, the mechanisms controlling t-tubule maintenance and whether these factors differ between species, cardiac chambers, and in a disease setting remain unclear.

objectiveTo determine the role of the Bin/Amphiphysin/Rvs domain protein amphiphysin II (AmpII) in regulating t-tubule maintenance and the systolic calcium transient. METHODS AND

resultsT-tubule density was assessed by di-4-ANEPPS, FM4-64 or WGA staining using confocal microscopy. In rat, ferret, and sheep hearts t-tubule density and AmpII protein levels were lower in the atrium than in the ventricle. Heart failure (HF) was induced in sheep using right ventricular tachypacing and ferrets by ascending aortic coarctation. In both HF models, AmpII protein and t-tubule density were decreased in the ventricles. In the sheep, atrial t-tubules were also lost in HF and AmpII levels decreased. Conversely, junctophilin 2 levels did not show interchamber differences in the rat and ferret nor did they change in HF in the sheep or ferret. In addition, in rat atrial and sheep HF atrial cells where t-tubules were absent, junctophilin 2 had sarcomeric intracellular distribution. Small interfering RNA-induced knockdown of AmpII protein reduced t-tubule density, calcium transient amplitude, and the synchrony of the systolic calcium transient.

conclusionsAmpII is intricately involved in t-tubule maintenance. Reducing AmpII protein decreases t-tubule density, reduces the amplitude, and increases the heterogeneity of the systolic calcium transient.

Indexed as

Excitation Contraction CouplingMyocardial ContractionAdaptor Proteins, Signal TransducingAnimalsCalciumCells, CulturedDisease Models, AnimalFerretsHeart AtriaHeart FailureHeart VentriclesMembrane ProteinsMicroscopy, ConfocalMyocytes, CardiacNerve Tissue ProteinsRatsAdaptor Proteins, Signal TransducingBin1 protein, ratCalciumjunctophilinMembrane ProteinsNerve Tissue ProteinsTumor Suppressor Proteinscalciumheart failure

Identifiers

PMID25332206
PMCPMC4274343
OpenAlexW2170643083

What OpenQuestion holds

Textmetadata
LicenceTDM
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.