Evidence map›Paper›PMID 12496068›Full record

ArticleBiophysical journal2002

An integrative model of the cardiac ventricular myocyte incorporating local control of Ca2+ release.

Joseph L Greenstein, Raimond L Winslow

Open access · bronzeAbstract read
In one paragraph

Article in Biophysical journal, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed
6.4field-weighted citation impact, top 3% 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

94 citing papers in PubMed, 200 citations in OpenAlex.

  1. Article
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  6. Review
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  9. Review
  10. CaBiophysical journal · 2020
    Article
  11. Article
  12. A bilobal model of CaThe Journal of general physiology · 2018
    Article
  13. Article
  14. Article
  15. Article
  16. Modeling NaJournal of molecular and cellular cardiology · 2016
    Article
  17. Article
  18. Article
  19. Electron tomography of rabbit cardiomyocyte three-dimensional ultrastructure.Progress in biophysics and molecular biology · 2016
    Article
  20. Article

34 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 1 institution in 1 country.

Joseph L GreensteinDepartment of Biomedical Engineering, Center for Computational Medicine and Biology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Raimond L Winslow
Johns Hopkins Medicine · US

Funding

Temporal and spatial variability of cardiac repolarizationP50HL052307 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI MARBAN, EDUARDO · 1995 to 2004
$10.0M
Calcium Entrained ArrhythmiasR01HL105239 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI JAFRI, MOHSIN SALEET, LEDERER, WILLIAM JONATHAN · 2011 to 2015
$4.9M
EXPERIMENTAL STUDY OF ARRHYTHMIAS IN HEART FAILURER01HL060133 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI WINSLOW, RAIMOND LESTER · 1998 to 2005
$1.4M
NHLBI NIH HHS P50 HL 52307NHLBI NIH HHS R01 HL060133NHLBI NIH HHS R01 HL105239NHLBI NIH HHS R01 HL 60133
6 · The paper itself

Abstract

The local control theory of excitation-contraction (EC) coupling in cardiac muscle asserts that L-type Ca(2+) current tightly controls Ca(2+) release from the sarcoplasmic reticulum (SR) via local interaction of closely apposed L-type Ca(2+) channels (LCCs) and ryanodine receptors (RyRs). These local interactions give rise to smoothly graded Ca(2+)-induced Ca(2+) release (CICR), which exhibits high gain. In this study we present a biophysically detailed model of the normal canine ventricular myocyte that conforms to local control theory. The model formulation incorporates details of microscopic EC coupling properties in the form of Ca(2+) release units (CaRUs) in which individual sarcolemmal LCCs interact in a stochastic manner with nearby RyRs in localized regions where junctional SR membrane and transverse-tubular membrane are in close proximity. The CaRUs are embedded within and interact with the global systems of the myocyte describing ionic and membrane pump/exchanger currents, SR Ca(2+) uptake, and time-varying cytosolic ion concentrations to form a model of the cardiac action potential (AP). The model can reproduce both the detailed properties of EC coupling, such as variable gain and graded SR Ca(2+) release, and whole-cell phenomena, such as modulation of AP duration by SR Ca(2+) release. Simulations indicate that the local control paradigm predicts stable APs when the L-type Ca(2+) current is adjusted in accord with the balance between voltage- and Ca(2+)-dependent inactivation processes as measured experimentally, a scenario where common pool models become unstable. The local control myocyte model provides a means for studying the interrelationship between microscopic and macroscopic behaviors in a manner that would not be possible in experiments.

Indexed as

Models, CardiovascularVentricular FunctionAction PotentialsAnimalsCalciumCalcium Channels, L-TypeComputer SimulationDogsIon Channel GatingMembrane PotentialsMuscle CellsMyocardial ContractionPatch-Clamp TechniquesRyanodine Receptor Calcium Release ChannelSarcoplasmic ReticulumCalciumCalcium Channels, L-TypeRyanodine Receptor Calcium Release Channel

Identifiers

PMID12496068
PMCPMC1201479
OpenAlexW2059424963

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.