The DOI matches its Crossref record; 14 of the 14 references it cites were found in a registry or an index.
Molecular Physiology of Cardiac Repolarization
Abstract
The heart is a rhythmic electromechanical pump, the functioning of which depends on action potential generation and propagation, followed by relaxation and a period of refractoriness until the next impulse is generated. Myocardial action potentials reflect the sequential activation and inactivation of inward (Na+and Ca 2+) and outward (K+) current carrying ion channels. In different regions of the heart, action potential waveforms are distinct, owing to differences in Na+, Ca 2+, and K+channel expression, and these differences contribute to the normal, unidirectional propagation of activity and to the generation of normal cardiac rhythms. Changes in channel functioning, resulting from inherited or acquired disease, affect action potential repolarization and can lead to the generation of life-threatening arrhythmias. There is, therefore, considerable interest in understanding the mechanisms that control cardiac repolarization and rhythm generation. Electrophysiological studies have detailed the properties of the Na+, Ca 2+, and K+currents that generate cardiac action potentials, and molecular cloning has revealed a large number of pore forming (α) and accessory (β, δ, and γ) subunits thought to contribute to the formation of these channels. Considerable progress has been made in defining the functional roles of the various channels and in identifying the α-subunits encoding these channels. Much less is known, however, about the functioning of channel accessory subunits and/or posttranslational processing of the channel proteins. It has also become clear that cardiac ion channels function as components of macromolecular complexes, comprising the α-subunits, one or more accessory subunit, and a variety of other regulatory proteins. In addition, these macromolecular channel protein complexes appear to interact with the actin cytoskeleton and/or the extracellular matrix, suggesting important functional links between channel complexes, as well as between cardiac structure and electrical functioning. Important areas of future research will be the identification of (all of) the molecular components of functional cardiac ion channels and delineation of the molecular mechanisms involved in regulating the expression and the functioning of these channels in the normal and the diseased myocardium.
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Citations
Cites
Structure and Regulation of Voltage-Gated Ca 2+ Channels
Catterall, W. A. (2000) · Annual Review of Cell and Developmental Biology · doi:10.1146/annurev.cellbio.16.1.521 · Cited by 2,344
CaV1.2 Calcium Channel Dysfunction Causes a Multisystem Disorder Including Arrhythmia and Autism
Splawski, I., Timothy, K. W., Sharpe, L. M., Decher, N., Kumar, P., Bloise, R., Napolitano, C., Schwartz, P. J., Joseph, R. M., Condouris, K., et al. (2004) · Cell · doi:10.1016/j.cell.2004.09.011 · Cited by 1,586 · cited 10×
“2a (479) demonstrates, as likely would have been”
BackgroundInfluentialStargazin regulates synaptic targeting of AMPA receptors by two distinct mechanisms
Chen, L., Chetkovich, D. M., Petralia, R. S., Sweeney, N. T., Kawasaki, Y., Wenthold, R. J., Bredt, D. S., & Nicoll, R. A. (2000) · Nature · doi:10.1038/35050030 · Cited by 1,111
A Potassium Channel Mutation in Neonatal Human Epilepsy
Biervert, C., Schroeder, B. C., Kubisch, C., Berkovic, S. F., Propping, P., Jentsch, T. J., & Steinlein, O. K. (1998) · Science · doi:10.1126/science.279.5349.403 · Cited by 1,073
Ankyrin-B mutation causes type 4 long-QT cardiac arrhythmia and sudden cardiac death
Mohler, P. J., Schott, J.-J., Gramolini, A. O., Dilly, K. W., Guatimosim, S., duBell, W. H., Song, L.-S., Haurogné, K., Kyndt, F., Ali, M. E., et al. (2003) · Nature · doi:10.1038/nature01335 · Cited by 957
Sudden death associated with short-QT syndrome linked to mutations in HERG
Brugada, R., Hong, K., Dumaine, R., Cordeiro, J., Gaita, F., Borggrefe, M., Menendez, T. M., Brugada, J., Pollevick, G. D., Wolpert, C., et al. (2004) · Circulation · doi:10.1161/01.cir.0000109482.92774.3a · Cited by 847
The sinoatrial node, a heterogeneous pacemaker structure
Boyett, M. (2000) · Cardiovascular Research · doi:10.1016/s0008-6363(00)00135-8 · Cited by 698
Overview of the voltage-gated sodium channel family
Yu (2003) · Genome biology · doi:10.1186/gb-2003-4-3-207 · Cited by 694
TREK-1, a K+ channel involved in neuroprotection and general anesthesia
Heurteaux, C., Guy, N., Laigle, C., Blondeau, N., Duprat, F., Mazzuca, M., Lang‐Lazdunski, L., Widmann, C., Zanzouri, M., Romey, G., et al. (2004) · The EMBO Journal · doi:10.1038/sj.emboj.7600234 · Cited by 534
Abbott, G. W., Butler, M. H., Bendahhou, S., Dalakas, M. C., Ptacek, L. J., & Goldstein, S. A. N. (2001) · Cell · doi:10.1016/s0092-8674(01)00207-0 · Cited by 294
Structure of a voltage-dependent K+ channel β subunit
Gulbis, J. M., Mann, S., & MacKinnon, R. (1999) · Cell · doi:10.1016/s0092-8674(00)80805-3 · Cited by 283
Channelopathies as a genetic cause of epilepsy
Mulley, J. C., Scheffer, I. E., Petrou, S., & Berkovic, S. F. (2003) · Current Opinion in Neurology · doi:10.1097/00019052-200304000-00009 · Cited by 214
Kamiya, K., Kaneda, M., Sugawara, T., Mazaki, E., Okamura, N., Montal, M., Makita, N., Tanaka, M., Fukushima, K., Fujiwara, T., et al. (2004) · The Journal of Neuroscience · doi:10.1523/jneurosci.3089-03.2004 · Cited by 199
Akar, F. G., Wu, R. C., Deschenes, I., Armoundas, A. A., Piacentino, V., Houser, S. R., & Tomaselli, G. F. (2004) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00673.2003 · Cited by 88
Cited by
Modernized Classification of Cardiac Antiarrhythmic Drugs
Lei, M., Wu, L., Terrar, D. A., & Huang, C. L.-H. (2018) · Circulation · doi:10.1161/circulationaha.118.035455 · Cited by 319
Crude Oil Impairs Cardiac Excitation-Contraction Coupling in Fish
Brette, F., Machado, B., Cros, C., Incardona, J. P., Scholz, N. L., & Block, B. A. (2014) · Science · doi:10.1126/science.1242747 · Cited by 310
Human engineered heart tissue as a model system for drug testing
Eder, A., Vollert, I., Hansen, A., & Eschenhagen, T. (2016) · Advanced Drug Delivery Reviews · doi:10.1016/j.addr.2015.05.010 · Cited by 190
Mechanisms of Sudden Cardiac Death: Oxidants and Metabolism
Yang, K.-C., Kyle, J. W., Makielski, J. C., & Dudley, S. C. (2015) · Circulation Research · doi:10.1161/circresaha.116.304691 · Cited by 127
QT Interval Screening in Methadone Maintenance Treatment: Report of a SAMHSA Expert Panel
Martin, J. A., Campbell, A., Killip, T., Kotz, M., Krantz, M. J., Kreek, M. J., McCarroll, B. A., Mehta, D., Payte, J. T., Stimmel, B., et al. (2011) · Journal of Addictive Diseases · doi:10.1080/10550887.2011.610710 · Cited by 87
“32 A QT interval of 390 to 420 ms in men or 400 to 440 ms in women is considered normal ( Figure 1 ).”
Background
Metadata
- Authors
- Nerbonne, J. M., & Kass, R. S.
- Venue
- Physiological Reviews
- Publisher
- American Physiological Society
- Published
- 2005-10
- Volume
- 85
- Issue
- 4
- Pages
- 1205-1253
- ISSN
- 0031-9333 (ISSN-L)
- 1522-1210
- OpenAlex
- W2165564780
- Cited by
- 1,062
- References
- 14
- FWCI
- 5.23
- Type
- journal article
- Language
- en
- Open access
- closed
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