Evidence map›Paper›PMID 22261047›Full record

ArticleBiophysical journal2011

A three-dimensional simulation model of cardiomyocyte integrating excitation-contraction coupling and metabolism.

Asuka Hatano, Jun-ichi Okada, Takumi Washio, Toshiaki Hisada, Seiryo Sugiura

Abstract read
In one paragraph

Article in Biophysical journal, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
–field-weighted citation impact
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

30 citing papers in PubMed.

  1. Cardiac myofibril networks induce shear stress.NPJ systems biology and applications · 2026
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  11. Clinical and pharmacological application of multiscale multiphysics heart simulator, UT-Heart.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2019
    Review
  12. Quantitative systems models illuminate arrhythmia mechanisms in heart failure: Role of the NaWiley interdisciplinary reviews. Systems biology and medicine · 2019
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Sarcoplasmic reticulum CaJournal of molecular and cellular cardiology · 2017
    Article
  19. Article
  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

5 authors.

Asuka HatanoDepartment of Frontier Science, The University of Tokyo, Kashiwa, Chiba, Japan. asuka-h@sml.k.u-tokyo.ac.jp
Jun-ichi Okada
Takumi Washio
Toshiaki Hisada
Seiryo Sugiura

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies have revealed that Ca(2+) not only regulates the contraction of cardiomyocytes, but can also function as a signaling agent to stimulate ATP production by the mitochondria. However, the spatiotemporal resolution of current experimental techniques limits our investigative capacity to understand this phenomenon. Here, we created a detailed three-dimensional (3D) cardiomyocyte model to study the subcellular regulatory mechanisms of myocardial energetics. The 3D cardiomyocyte model was based on the finite-element method, with detailed subcellular structures reproduced, and it included all elementary processes involved in cardiomyocyte electrophysiology, contraction, and ATP metabolism localized to specific loci. The simulation results were found to be reproducible and consistent with experimental data regarding the spatiotemporal pattern of cytosolic, intrasarcoplasmic-reticulum, and mitochondrial changes in Ca(2+); as well as changes in metabolite levels. Detailed analysis suggested that although the observed large cytosolic Ca(2+) gradient facilitated uptake by the mitochondrial Ca(2+) uniporter to produce cyclic changes in mitochondrial Ca(2+) near the Z-line region, the average mitochondrial Ca(2+) changes slowly. We also confirmed the importance of the creatine phosphate shuttle in cardiac energy regulation. In summary, our 3D model provides a powerful tool for the study of cardiac function by overcoming some of the spatiotemporal limitations of current experimental approaches.

Indexed as

Computer SimulationModels, BiologicalAdenine Nucleotide Translocator 1Adenosine DiphosphateBiomechanical PhenomenaCalciumCalcium SignalingCytosolEnergy MetabolismExcitation Contraction CouplingMitochondriaMyocytes, CardiacMyofibrilsSarcomeresTime-Lapse ImagingAdenine Nucleotide Translocator 1Adenosine DiphosphateCalcium

Identifiers

PMID22261047
PMCPMC3297787

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.