Evidence map›Paper›PMID 25928268›Full record

ArticlePLoS computational biology2015

Cell-specific cardiac electrophysiology models.

Willemijn Groenendaal, Francis A Ortega, Armen R Kherlopian, Andrew C Zygmunt, Trine Krogh-Madsen, David J Christini

Abstract read
In one paragraph

Article in PLoS computational biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing 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

67 citing papers in PubMed.

  1. Trial
  2. Article
  3. Article
  4. Large-scale synthetic data enable digital twins of human excitable cells.bioRxiv : the preprint server for biology · 2025
    Article
  5. Article
  6. Article
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  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Computational Modeling of Cardiac Electrophysiology.Methods in molecular biology (Clifton, N.J.) · 2024
    Article
  17. Article
  18. Article
  19. Article
  20. Article

7 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

6 authors.

Willemijn GroenendaalGreenberg Division of Cardiology, Weill Cornell Medical College, New York, New York, United States of America.
Francis A OrtegaDepartment of Physiology and Biophysics, Weill Cornell Medical College, New York, New York, United States of America.
Armen R KherlopianDepartment of Physiology and Biophysics, Weill Cornell Medical College, New York, New York, United States of America.
Andrew C ZygmuntConsultant, New Hartford, New York, United States of America.
Trine Krogh-MadsenGreenberg Division of Cardiology, Weill Cornell Medical College, New York, New York, United States of America; Institute for Computational Biomedicine, Weill Cornell Medical College, New York, New York, United States of America.
David J ChristiniGreenberg Division of Cardiology, Weill Cornell Medical College, New York, New York, United States of America; Department of Physiology and Biophysics, Weill Cornell Medical College, New York, New York, United States of America; Institute for Computational Biomedicine, Weill Cornell Medical College, New York, New York, United States of America.

Funding

Real-time control system for biological experimentsR01EB016407 · NIBIB · WEILL MEDICAL COLL OF CORNELL UNIV · PI CHRISTINI, DAVID J. · 2013 to 2016
$2.7M
NIBIB NIH HHS R01 EB016407NIBIB NIH HHS R01EB016407
6 · The paper itself

Abstract

The traditional cardiac model-building paradigm involves constructing a composite model using data collected from many cells. Equations are derived for each relevant cellular component (e.g., ion channel, exchanger) independently. After the equations for all components are combined to form the composite model, a subset of parameters is tuned, often arbitrarily and by hand, until the model output matches a target objective, such as an action potential. Unfortunately, such models often fail to accurately simulate behavior that is dynamically dissimilar (e.g., arrhythmia) to the simple target objective to which the model was fit. In this study, we develop a new approach in which data are collected via a series of complex electrophysiology protocols from single cardiac myocytes and then used to tune model parameters via a parallel fitting method known as a genetic algorithm (GA). The dynamical complexity of the electrophysiological data, which can only be fit by an automated method such as a GA, leads to more accurately parameterized models that can simulate rich cardiac dynamics. The feasibility of the method is first validated computationally, after which it is used to develop models of isolated guinea pig ventricular myocytes that simulate the electrophysiological dynamics significantly better than does a standard guinea pig model. In addition to improving model fidelity generally, this approach can be used to generate a cell-specific model. By so doing, the approach may be useful in applications ranging from studying the implications of cell-to-cell variability to the prediction of intersubject differences in response to pharmacological treatment.

Indexed as

Models, CardiovascularAction PotentialsAnimalsCells, CulturedComputer SimulationHeart Conduction SystemIon Channel GatingIon ChannelsMembrane PotentialsModels, StatisticalMyocytes, CardiacSwineIon Channels

Identifiers

PMID25928268
PMCPMC4415772

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.