Studying cardiac arrhythmias in the mouse—a reasonable model for probing mechanisms?

Nerbonne, J

doi:10.1016/j.tcm.2003.12.006

Cited by 175Cardiac electrophysiology and arrhythmiasIon channel regulation and functionCardiac Arrhythmias and Treatments

Studying cardiac arrhythmias in the mouse—a reasonable model for probing mechanisms?

Nerbonne, J·2004·Trends in Cardiovascular Medicine

DOI 10.1016/j.tcm.2003.12.006

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Abstract

The normal mechanical functioning of the heart depends on proper electrical functioning, reflected in the sequential activation of pacemaker cells, and the normal propagation of activity through the ventricles. Myocardial electrical activity is evident in the form of action potentials, reflecting the activation (and inactivation) of depolarizing (Na(+), Ca(2+)) and repolarizing (K(+)) current channels. There are multiple types of myocardial K(+) channels, contributing to regional differences in action potential waveforms and to the generation of normal cardiac rhythms. The conduction and propagation of activity through the myocardium depends on electrical coupling between cells, mediated by gap junction channels. In the diseased myocardium, action potential waveforms and conduction are affected markedly, owing to changes in the functional expression of repolarizing K(+) and other channels. These changes can lead to desynchronization of the heart and to arrhythmia generation. There is presently greater interest in defining the cellular, molecular, and systemic mechanisms contributing to the generation and the maintenance of cardiac arrhythmias. Although a variety of experimental (animal) model systems have been (and are being) exploited in these efforts, the mouse is being used increasingly, due to the ease with which molecular genetic strategies can be applied. The important issue is whether the mouse is an appropriate model system to explore arrhythmia mechanisms.

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Mouse action potentials have rapid repolarization and lack a prominent plateau phase found in human cardiomyocytes.
“Mouse action potentials have a rapid repolarization and lack a prominent plateau phase which is found in human cardiomyocytes”
From Small and large animal models in cardiac contraction research: advantages and disadvantages (2014) · cites this paper as Nerbonne, 2004

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Self-citation

Authors: Nerbonne, J.
Affiliations: Washington University in St. Louis (US)
Corresponding author: Nerbonne, J
ORCID: Nerbonne, J
Venue: Trends in Cardiovascular Medicine
Publisher: Elsevier BV
Published: 2004-04
Volume: 14
Issue: 3
Pages: 83-93
ISSN: 1050-1738 (ISSN-L)
DOI: 10.1016/j.tcm.2003.12.006
OpenAlex: W2039577288
Cited by: 175
References: 59
Citations by year: 2026: 2 · 2025: 5 · 2024: 4 · 2023: 9 · 2022: 4 · 2021: 14 · 2020: 9 · 2019: 7 · 2018: 11 · 2017: 9 · 2016: 13 · 2015: 7 · 2014: 13 · 2013: 8 · 2012: 13
FWCI: 4.61
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Trends in Cardiovascular Medicine (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac electrophysiology and arrhythmias
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Arrhythmias and Treatments
Keywords: cardiac arrhythmias, mouse model, action potential, potassium channels, gap junctions, cardiac electrophysiology, cardiac conduction, repolarization, arrhythmia mechanisms, molecular genetics
MeSH terms: ERG1 Potassium Channel, Action Potentials, Animals, Arrhythmias, Cardiac, Disease Models, Animal, Heart, Heart Conduction System, Heart Ventricles, Humans, Long QT Syndrome, Mice, Transgenic, Potassium Channels, 4-Aminopyridine, Ventricular Function, Potassium Channels, Voltage-Gated, Potassium Channel Blockers, Myocytes, Cardiac, Mice, Ether-A-Go-Go Potassium Channels, KCNQ Potassium Channels, KCNQ1 Potassium Channel, Kv1.1 Potassium Channel, Shal Potassium Channels

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Studying cardiac arrhythmias in the mouse—a reasonable model for probing mechanisms?

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