Evidence map›Paper›PMID 16848931›Full record

ReviewQuarterly reviews of biophysics2006

Computational biology in the study of cardiac ion channels and cell electrophysiology.

Yoram Rudy, Jonathan R Silva

Open access · greenAbstract readReview
In one paragraph

Review in Quarterly reviews of biophysics, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
102citing papers in PubMed, 1 pooled it
11.9field-weighted citation impact, top 1% 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

102 citing papers in PubMed, 1 synthesis or guideline pooled it, 273 citations in OpenAlex.

  1. Guideline
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  3. Article
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  7. Article
  8. Article
  9. Evaluating the predictive accuracy of ion-channel models using data from multiple experimental designs.Philosophical transactions. Series A, Mathematical, physical, and engineering sciences · 2025
    Article
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  11. Review
  12. Article
  13. Review
  14. Article
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  16. Review
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  18. Review
  19. Article
  20. Article

42 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

2 authors at 2 institutions in 1 country.

Yoram RudyCardiac Bioelectricity & Arrhythmia Center, Department of Biomedical Engineering, Washington University, St. Louis, MO 63130-489, USA. rudy@wustl.edu
Jonathan R Silva
Texas Cardiac Arrhythmia · USWashington University in St. Louis · US

Funding

CARDIAC EXCITATION AND ARRHYTHMIASR01HL049054 · NHLBI · WASHINGTON UNIVERSITY · PI RUDY, YORAM · 1993 to 2017
$5.8M
INVERSE AND FORWARD PROBLEMS IN ELECTROCARDIOGRAPHYR37HL033343 · NHLBI · WASHINGTON UNIVERSITY · PI RUDY, YORAM · 1998 to 2007
$2.0M
Single Ion Channel Determines Phenotype from GenotypeF31HL068318 · NHLBI · WASHINGTON UNIVERSITY · PI SILVA, JONATHAN R · 2001 to 2005
$157k
NHLBI NIH HHS F31 HL068318NHLBI NIH HHS F31-HL68313NHLBI NIH HHS R01 HL049054NHLBI NIH HHS R01-HL49054NHLBI NIH HHS R37 HL033343NHLBI NIH HHS R37-HL33343
6 · The paper itself

Abstract

The cardiac cell is a complex biological system where various processes interact to generate electrical excitation (the action potential, AP) and contraction. During AP generation, membrane ion channels interact nonlinearly with dynamically changing ionic concentrations and varying transmembrane voltage, and are subject to regulatory processes. In recent years, a large body of knowledge has accumulated on the molecular structure of cardiac ion channels, their function, and their modification by genetic mutations that are associated with cardiac arrhythmias and sudden death. However, ion channels are typically studied in isolation (in expression systems or isolated membrane patches), away from the physiological environment of the cell where they interact to generate the AP. A major challenge remains the integration of ion-channel properties into the functioning, complex and highly interactive cell system, with the objective to relate molecular-level processes and their modification by disease to whole-cell function and clinical phenotype. In this article we describe how computational biology can be used to achieve such integration. We explain how mathematical (Markov) models of ion-channel kinetics are incorporated into integrated models of cardiac cells to compute the AP. We provide examples of mathematical (computer) simulations of physiological and pathological phenomena, including AP adaptation to changes in heart rate, genetic mutations in SCN5A and HERG genes that are associated with fatal cardiac arrhythmias, and effects of the CaMKII regulatory pathway and beta-adrenergic cascade on the cell electrophysiological function.

Indexed as

Action PotentialsBiophysical PhenomenaBiophysicsCalcium-Calmodulin-Dependent Protein KinasesCalcium-Calmodulin-Dependent Protein Kinase Type 2Calcium SignalingComputational BiologyComputer SimulationElectrophysiologyERG1 Potassium ChannelEther-A-Go-Go Potassium ChannelsHumansIon ChannelsKineticsMarkov ChainsModels, CardiovascularCalcium-Calmodulin-Dependent Protein KinasesCalcium-Calmodulin-Dependent Protein Kinase Type 2ERG1 Potassium ChannelEther-A-Go-Go Potassium ChannelsIon ChannelsKCNH2 protein, humanMuscle ProteinsNAV1.5 Voltage-Gated Sodium ChannelReceptors, Adrenergic, betaSCN5A protein, humanSodium Channels

Identifiers

PMID16848931
PMCPMC1994938
OpenAlexW2003251032

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.