Evidence map›Paper›PMID 28185290›Full record

ArticleThe Journal of physiology2017

Computational analysis of the human sinus node action potential: model development and effects of mutations.

Alan Fabbri, Matteo Fantini, Ronald Wilders, Stefano Severi

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
10.2field-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

57 citing papers in PubMed, 132 citations in OpenAlex.

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  10. A gain-of-function HCN4 mutant in the HCN domain is responsible for inappropriate sinus tachycardia in a Spanish family.Proceedings of the National Academy of Sciences of the United States of America · 2023
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  15. Regenerative therapy · 2022
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  16. Whole Exome Sequencing Identifies a Heterozygous Variant in the Cav1.3 GeneInternational journal of molecular sciences · 2022
    Article
  17. Article
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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

4 authors at 2 institutions in 2 countries.

Alan FabbriComputational Physiopathology Unit, Department of Electrical, Electronic and Information Engineering "Guglielmo Marconi", University of Bologna, Cesena, Italy.
Matteo FantiniComputational Physiopathology Unit, Department of Electrical, Electronic and Information Engineering "Guglielmo Marconi", University of Bologna, Cesena, Italy.
Ronald WildersDepartment of Anatomy, Embryology and Physiology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.ORCID 0000-0002-1340-0869
Stefano SeveriComputational Physiopathology Unit, Department of Electrical, Electronic and Information Engineering "Guglielmo Marconi", University of Bologna, Cesena, Italy.ORCID 0000-0003-4306-8294
Marconi University · ITAmsterdam UMC Location University of Amsterdam · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

key pointsWe constructed a comprehensive mathematical model of the spontaneous electrical activity of a human sinoatrial node (SAN) pacemaker cell, starting from the recent Severi-DiFrancesco model of rabbit SAN cells. Our model is based on electrophysiological data from isolated human SAN pacemaker cells and closely matches the action potentials and calcium transient that were recorded experimentally. Simulated ion channelopathies explain the clinically observed changes in heart rate in corresponding mutation carriers, providing an independent qualitative validation of the model. The model shows that the modulatory role of the 'funny current' (I ABSTRACT: The sinoatrial node (SAN) is the normal pacemaker of the mammalian heart.  Over several decades, a large amount of data on the ionic mechanisms underlying the spontaneous electrical activity of SAN pacemaker cells has been obtained, mostly in experiments on single cells isolated from rabbit SAN. This wealth of data has allowed the development of mathematical models of the electrical activity of rabbit SAN pacemaker cells. The present study aimed to construct a comprehensive model of the electrical activity of a human SAN pacemaker cell using recently obtained electrophysiological data from human SAN pacemaker cells.  We based our model on the recent Severi-DiFrancesco model of a rabbit SAN pacemaker cell. The action potential and calcium transient of the resulting model are close to the experimentally recorded values. The model has a much smaller 'funny current' (I

Indexed as

Models, BiologicalAction PotentialsAnimalsHeart RateHumansIon ChannelsMutationMyocytes, CardiacRabbitsSinoatrial NodeIon Channelsaction potentialscardiac electrophysiologycardiomyocytecardiovascular modelscomputer simulationheart ratehumanion channelssinoatrial node

Identifiers

PMID28185290
PMCPMC5374121
OpenAlexW2586672809

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.