The DOI matches its Crossref record; 59 of the 59 references it cites were found in a registry or an index.
Studying Cardiac Arrhythmias in the Mouse—A Reasonable Model for Probing Mechanisms?
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 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
Citations
Cites
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KvLQT1 and IsK (minK) proteins associate to form the IKS cardiac potassium current
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KCNQ1 Gain-of-Function Mutation in Familial Atrial Fibrillation
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Modulation of A-type potassium channels by a family of calcium sensors
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Cited by
Sorted by citations
Voltage-gated potassium channels as therapeutic targets
Wulff, H., Castle, N. A., & Pardo, L. A. (2009) · Nature Reviews Drug Discovery · doi:10.1038/nrd2983 · Cited by 810
Small and large animal models in cardiac contraction research: advantages and disadvantages
Milani-Nejad, N., & Janssen, P. M. L. (2014) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2013.10.007 · Cited by 484
Denning, C., Borgdorff, V., Crutchley, J., Firth, K. S. A., George, V., Kalra, S., Kondrashov, A., Hoang, M. D., Mosqueira, D., Patel, A., et al. (2016) · Biochimica et Biophysica Acta (BBA) - Molecular Cell Research · doi:10.1016/j.bbamcr.2015.10.014 · Cited by 293
“associated with increased force of contraction in humans but decreased force in mice [17].”
BackgroundZebrafish model for human long QT syndrome
Arnaout, R., Ferrer, T., Huisken, J., Spitzer, K. W., Stainier, D. Y. R., Tristani‐Firouzi, M., & Chi, N. C. (2007) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0702724104 · Cited by 240
Musunuru, K., Sheikh, F., Gupta, R. M., Houser, S. R., Maher, K., Milan, D. J., Terzic, A., & Wu, J. C. (2018) · Circulation Genomic and Precision Medicine · doi:10.1161/hcg.0000000000000043 · Cited by 237
Metadata
- 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)
- 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
- 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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