Evidence map›Paper›PMID 23671664›Full record

ArticlePloS one2013

A mathematical model of the mouse ventricular myocyte contraction.

Paula D Mullins, Vladimir E Bondarenko

Abstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Transmural cellular heterogeneity in myocardial electromechanics.The journal of physiological sciences : JPS · 2018
    Article
  6. Article
  7. Review
  8. Biomechanics of Cardiac Function.Comprehensive Physiology · 2015
    Review
  9. Review
  10. Article
  11. Review
  12. 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

2 authors.

Paula D MullinsDepartment of Mathematics and Statistics, Georgia State University, Atlanta, Georgia, USA.
Vladimir E Bondarenko

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mathematical models of cardiac function at the cellular level include three major components, such as electrical activity, Ca(2+) dynamics, and cellular shortening. We developed a model for mouse ventricular myocyte contraction which is based on our previously published comprehensive models of action potential and Ca(2+) handling mechanisms. The model was verified with extensive experimental data on mouse myocyte contraction at room temperature. In the model, we implemented variable sarcomere length and indirect modulation of the tropomyosin transition rates by Ca(2+) and troponin. The resulting model described well steady-state force-calcium relationships, dependence of the contraction force on the sarcomere length, time course of the contraction force and myocyte shortening, frequency dependence of the contraction force and cellular contraction, and experimentally measured derivatives of the myocyte length variation. We emphasized the importance of the inclusion of variable sarcomere length into a model for ventricular myocyte contraction. Differences in contraction force and cell shortening for epicardial and endocardial ventricular myocytes were investigated. Model applicability for the experimental studies and model limitations were discussed.

Indexed as

AlgorithmsModels, CardiovascularAnimalsCalciumCalcium Channels, L-TypeHeart VentriclesMarkov ChainsMembrane PotentialsMiceMyocardial ContractionMyocytes, CardiacSarcomeresSodium ChannelsTropomyosinTroponinCalciumCalcium Channels, L-TypeSodium ChannelsTropomyosinTroponin

Identifiers

PMID23671664
PMCPMC3650013

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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.