Evidence map›Paper›PMID 23846763›Full record

ReviewCellular and molecular life sciences : CMLS2013

The transverse-axial tubular system of cardiomyocytes.

C Ferrantini, C Crocini, R Coppini, F Vanzi, C Tesi, E Cerbai, C Poggesi, F S Pavone, L Sacconi

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
4.7field-weighted citation impact, top 4% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.

  1. Engineering the maturation of stem cell-derived cardiomyocytes.Frontiers in bioengineering and biotechnology · 2023
    Pooled it
  2. Review
  3. Role of ryanodine receptor cooperativity in CaThe Journal of physiology · 2024
    Article
  4. Article
  5. Postprandial cardiac hypertrophy is sustained by mechanics, epigenetic, and metabolic reprogramming in pythons.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  6. Article
  7. Differences in Effects of Length-Dependent Regulation of Force and CaInternational journal of molecular sciences · 2023
    Article
  8. Role of CaArchives of toxicology · 2023
    Review
  9. Review
  10. T-tubule remodeling in human hypertrophic cardiomyopathy.Journal of muscle research and cell motility · 2021
    Review
  11. Article
  12. Calcium Signaling in Cardiomyocyte Function.Cold Spring Harbor perspectives in biology · 2020
    Review
  13. Article
  14. Reply to Entcheva: The impact of T-tubules on action potential propagation in cardiac tissue.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  15. Altered CaFrontiers in physiology · 2018
    Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

9 authors at 1 institution in 1 country.

C FerrantiniDivision of Physiology, Department of Clinical and Experimental Medicine, University of Florence, Florence, Italy.
C Crocini
R Coppini
F Vanzi
C Tesi
E Cerbai
C Poggesi
F S Pavone
L Sacconi
University of Florence · IT

Funding

Telethon GGP13162
6 · The paper itself

Abstract

A characteristic histological feature of striated muscle cells is the presence of deep invaginations of the plasma membrane (sarcolemma), most commonly referred to as T-tubules or the transverse-axial tubular system (TATS). TATS mediates the rapid spread of the electrical signal (action potential) to the cell core triggering Ca(2+) release from the sarcoplasmic reticulum, ultimately inducing myofilament contraction (excitation-contraction coupling). T-tubules, first described in vertebrate skeletal muscle cells, have also been recognized for a long time in mammalian cardiac ventricular myocytes, with a structure and a function that in recent years have been shown to be far more complex and pivotal for cardiac function than initially thought. Renewed interest in T-tubule function stems from the loss and disorganization of T-tubules found in a number of pathological conditions including human heart failure (HF) and dilated and hypertrophic cardiomyopathies, as well as in animal models of HF, chronic ischemia and atrial fibrillation. Disease-related remodeling of the TATS leads to asynchronous and inhomogeneous Ca(2+)-release, due to the presence of orphan ryanodine receptors that have lost their coupling with the dihydropyridine receptors and are either not activated or activated with a delay. Here, we review the physiology of the TATS, focusing first on the relationship between function and structure, and then describing T-tubular remodeling and its reversal in disease settings and following effective therapeutic approaches.

Indexed as

Action PotentialsAnimalsArrhythmias, CardiacCalcium SignalingExcitation Contraction CouplingHeart DiseasesHumansModels, CardiovascularMyocardial ContractionMyocytes, CardiacSarcolemma

Identifiers

PMID23846763
PMCPMC11113601
OpenAlexW2137671098

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.