Evidence map›Paper›PMID 16679365›Full record

ArticleBiophysical journal2006

A computational model integrating electrophysiology, contraction, and mitochondrial bioenergetics in the ventricular myocyte.

Sonia Cortassa, Miguel A Aon, Brian O'Rourke, Robert Jacques, Hsiang-Jer Tseng, Eduardo Marbán, Raimond L Winslow

Open access · bronzeAbstract read
In one paragraph

Article in Biophysical journal, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers.

0numbers the graph read from it
0cells of the map it votes in
105citing papers in PubMed
5.8field-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

105 citing papers in PubMed, 207 citations in OpenAlex.

  1. A Computational Model of Oxidative Stress in a Human Ventricular Myocyte.bioRxiv : the preprint server for biology · 2026
    Article
  2. Mechanistic Modeling of MCUx Gatekeeping, CaAmerican journal of physiology. Cell physiology · 2026
    Article
  3. Article
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  8. CaFrontiers in physiology · 2023
    Article
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  11. Review
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  14. Observational
  15. Mitochondrial CaInternational journal of molecular sciences · 2022
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

45 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

7 authors at 1 institution in 1 country.

Sonia CortassaThe Johns Hopkins University, Institute for Computational Medicine, and Institute of Molecular Cardiobiology, Baltimore, Maryland 21218, USA.
Miguel A Aon
Brian O'Rourke
Robert Jacques
Hsiang-Jer Tseng
Eduardo Marbán
Raimond L Winslow
Johns Hopkins University · US

Funding

STRUCTURE OF MITOCHONDRIAL K+ CHANNELSP01HL081427 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI VAN EYK, JENNIFER E · 2005 to 2009
$11.2M
ENERGETIC REGULATION OF CARDIAC ION CHANNELSR37HL054598 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI O'ROURKE, BRIAN · 2005 to 2014
$3.7M
NHLBI NIH HHS P01 HL081427NHLBI NIH HHS R37 HL054598
6 · The paper itself

Abstract

An intricate network of reactions is involved in matching energy supply with demand in the heart. This complexity arises because energy production both modulates and is modulated by the electrophysiological and contractile activity of the cardiac myocyte. Here, we present an integrated mathematical model of the cardiac cell that links excitation-contraction coupling with mitochondrial energy generation. The dynamics of the model are described by a system of 50 ordinary differential equations. The formulation explicitly incorporates cytoplasmic ATP-consuming processes associated with force generation and ion transport, as well as the creatine kinase reaction. Changes in the electrical and contractile activity of the myocyte are coupled to mitochondrial energetics through the ATP, Ca2+, and Na+ concentrations in the myoplasmic and mitochondrial matrix compartments. The pseudo steady-state relationship between force and oxygen consumption at various stimulus frequencies and external Ca2+ concentrations is reproduced in both model simulations and direct experiments in cardiac trabeculae under normoxic conditions, recapitulating the linearity between cardiac work and respiration in the heart. Importantly, the model can also reproduce the rapid time-dependent changes in mitochondrial NADH and Ca2+ in response to abrupt changes in workload. The steady-state and dynamic responses of the model were conferred by ADP-dependent stimulation of mitochondrial oxidative phosphorylation and Ca2+ -dependent regulation of Krebs cycle dehydrogenases, illustrating how the model can be used as a tool for investigating mechanisms underlying metabolic control in the heart.

Indexed as

Models, CardiovascularVentricular FunctionAction PotentialsCalcium SignalingComputer SimulationElectrophysiologyEnergy MetabolismHeart Conduction SystemMitochondriaMyocardial ContractionMyocytes, CardiacStress, Mechanical

Identifiers

PMID16679365
PMCPMC1518641
OpenAlexW1964430604

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.