Evidence map›Paper›PMID 18408122›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2008

Mathematical model of the neonatal mouse ventricular action potential.

Linda J Wang, Eric A Sobie

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

32 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Calcium-dependent inactivation controls cardiac L-type CaThe Journal of general physiology · 2019
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. The cardiac L-type calcium channel distal carboxy terminus autoinhibition is regulated by calcium.American journal of physiology. Heart and circulatory physiology · 2013
    Article
  15. Article
  16. Article
  17. At the heart of computational modelling.The Journal of physiology · 2012
    Review
  18. Article
  19. An introduction to dynamical systems.Science signaling · 2011
    Article
  20. 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 at 1 institution in 1 country.

Linda J WangDepartment of Pharmacology and Systems Therapeutics, Mount Sinai School of Medicine, New York, New York, USA.
Eric A Sobie
Icahn School of Medicine at Mount Sinai · US

Funding

System Biology Center in New YorkP50GM071558 · NIGMS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI ZAPH, SUSANA NEVES · 2007 to 2017
$22.8M
Sarcoplasmic reticulum calcium leak and calcium instability in cardiac myocytesR01HL076230 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI SOBIE, ERIC A · 2005 to 2013
$3.0M
NHLBI NIH HHS HL076230NHLBI NIH HHS R01 HL076230NIGMS NIH HHS P50 GM071558
6 · The paper itself

Abstract

Therapies for heart disease are based largely on our understanding of the adult myocardium. The dramatic differences in action potential (AP) shape between neonatal and adult cardiac myocytes, however, indicate that a different set of molecular interactions in neonatal myocytes necessitates different treatment for newborns. Computational modeling is useful for synthesizing data to determine how interactions between components lead to systems-level behavior, but this technique has not been used extensively to study neonatal heart cell function. We created a mathematical model of the neonatal (day 1) mouse myocyte by modifying, on the basis of experimental data, the densities and/or formulations of ion transport mechanisms in an adult cell model. The new model reproduces the characteristic AP shape of neonatal cells, with a brief plateau phase and longer duration than the adult (action potential duration at 80% repolarization = 60.1 vs. 12.6 ms). The simulation results are consistent with experimental data, including 1) decreased density and altered inactivation of transient outward K+ currents, 2) increased delayed rectifier K+ currents, 3) Ca2+ entry through T-type as well as L-type Ca2+ channels, 4) increased Ca2+ influx through Na+/Ca2+ exchange, and 5) Ca2+ transients resulting from transmembrane Ca2+ entry rather than release from the sarcoplasmic reticulum (SR). Simulations performed with the model generated novel predictions, including increased SR Ca2+ leak and elevated intracellular Na+ concentration in neonatal compared with adult myocytes. This new model can therefore be used for testing hypotheses and obtaining a better quantitative understanding of differences between neonatal and adult physiology.

Indexed as

Action PotentialsComputer SimulationModels, CardiovascularAnimalsAnimals, NewbornCalciumCalcium Channels, L-TypeCalcium SignalingDelayed Rectifier Potassium ChannelsHeart VentriclesMiceMyocytes, CardiacPotassiumRatsSarcoplasmic ReticulumSodiumCalciumCalcium Channels, L-TypeDelayed Rectifier Potassium ChannelsPotassiumSodiumSodium-Calcium Exchanger

Identifiers

PMID18408122
PMCPMC3032983
OpenAlexW2098457073

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.