Evidence map›Paper›PMID 23100327›Full record

ArticleHuman molecular genetics2013

A critical role for Telethonin in regulating t-tubule structure and function in the mammalian heart.

Michael Ibrahim, Urszula Siedlecka, Byambajav Buyandelger, Mutsuo Harada, Christopher Rao, Alexey Moshkov, Anamika Bhargava, Michael Schneider, Magdi H Yacoub, Julia Gorelik and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Human molecular genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

38 citing papers in PubMed, 67 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Muscular Dystrophies.Advances in experimental medicine and biology · 2025
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Frontiers in cell and developmental biology · 2022
    Article
  13. T-tubule remodeling in human hypertrophic cardiomyopathy.Journal of muscle research and cell motility · 2021
    Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Calcium Signaling in Cardiomyocyte Function.Cold Spring Harbor perspectives in biology · 2020
    Review
  19. Article
  20. Dyadic Plasticity in Cardiomyocytes.Frontiers in physiology · 2018
    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

12 authors at 2 institutions in 1 country.

Michael IbrahimLaboratory of Cell Electrophysiology, Heart Science Centre, Harefield Hospital, London UB9 6JH, UK.
Urszula Siedlecka
Byambajav Buyandelger
Mutsuo Harada
Christopher Rao
Alexey Moshkov
Anamika Bhargava
Michael Schneider
Magdi H Yacoub
Julia Gorelik
Ralph Knöll
Cesare M Terracciano
Harefield Hospital · GBImperial College London · GB

Funding

British Heart Foundation FS/09/025/27468British Heart Foundation FS/12/76/29859British Heart Foundation NH/10/3/28574British Heart Foundation PG/11/34/28793British Heart Foundation PG11/34/28793British Heart Foundation RE/08/002British Heart Foundation RG/11/20/29266Wellcome Trust WTN090594
6 · The paper itself

Abstract

The transverse (t)-tubule system plays an essential role in healthy and diseased heart muscle, particularly in Ca(2+)-induced Ca(2+) release (CICR), and its structural disruption is an early event in heart failure. Both mechanical overload and unloading alter t-tubule structure, but the mechanisms mediating the normally tight regulation of the t-tubules in response to load variation are poorly understood. Telethonin (Tcap) is a stretch-sensitive Z-disc protein that binds to proteins in the t-tubule membrane. To assess its role in regulating t-tubule structure and function, we used Tcap knockout (KO) mice and investigated cardiomyocyte t-tubule and cell structure and CICR over time and following mechanical overload. In cardiomyocytes from 3-month-old KO (3mKO), there were isolated t-tubule defects and Ca(2+) transient dysynchrony without whole heart and cellular dysfunction. Ca(2+) spark frequency more than doubled in 3mKO. At 8 months of age (8mKO), cardiomyocytes showed progressive loss of t-tubules and remodelling of the cell surface, with prolonged and dysynchronous Ca(2+) transients. Ca(2+) spark frequency was elevated and the L-type Ca(2+) channel was depressed at 8 months only. After mechanical overload obtained by aortic banding constriction, the Ca(2+) transient was prolonged in both wild type and KO. Mechanical overload increased the Ca(2+) spark frequency in KO alone, where there was also significantly more t-tubule loss, with a greater deterioration in t-tubule regularity. In conjunction, Tcap KO showed severe loss of cell surface ultrastructure. These data suggest that Tcap is a critical, load-sensitive regulator of t-tubule structure and function.

Indexed as

AnimalsCalciumCalcium SignalingConnectinHeartMiceMice, KnockoutMuscle ProteinsMyocytes, CardiacSarcolemmaCalciumConnectinMuscle ProteinsTcap protein, mouse

Identifiers

PMID23100327
PMCPMC3526164
OpenAlexW2131236986

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.