The DOI matches its Crossref record; 230 of the 230 references it cites were found in a registry or an index.
Cardiac Ion Channels
Abstract
▪ Abstract The normal electrophysiologic behavior of the heart is determined by ordered propagation of excitatory stimuli that result in rapid depolarization and slow repolarization, thereby generating action potentials in individual myocytes. Abnormalities of impulse generation, propagation, or the duration and configuration of individual cardiac action potentials form the basis of disorders of cardiac rhythm, a continuing major public health problem for which available drugs are incompletetly effective and often dangerous. The integrated activity of specific ionic currents generates action potentials, and the genes whose expression results in the molecular components underlying individual ion currents in heart have been cloned. This review discusses these new tools and how their application to the problem of arrhythmias is generating new mechanistic insights to identify patients at risk for this condition and developing improved antiarrhythmic therapies.
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Citations
Cites
1 retracted
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Cited by
Genesis and Regulation of the Heart Automaticity
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Mechanisms of Sudden Cardiac Death: Oxidants and Metabolism
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Metadata
- Authors
- Roden, D. M., Balser, J. R., George Jr, A. L., & Anderson, M. E.
- Venue
- Annual Review of Physiology
- Publisher
- Annual Reviews
- Published
- 2002-03
- Volume
- 64
- Issue
- 1
- Pages
- 431-475
- ISSN
- 0066-4278 (ISSN-L)
- 1545-1585
- OpenAlex
- W2121912757
- Cited by
- 305
- References
- 230
- FWCI
- 1.76
- Type
- journal article
- Language
- en
- Open access
- closed
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- Roden, D. M., Balser, J. R., George Jr, A. L., & Anderson, M. E. (2002). Cardiac Ion Channels. Annual Review of Physiology. https://doi.org/10.1146/annurev.physiol.64.083101.145105
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
