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Calcium and Arrhythmogenesis
Open accessAbstract
Triggered activity in cardiac muscle and intracellular Ca 2+have been linked in the past. However, today not only are there a number of cellular proteins that show clear Ca 2+dependence but also there are a number of arrhythmias whose mechanism appears to be linked to Ca 2+-dependent processes. Thus we present a systematic review of the mechanisms of Ca 2+transport (forward excitation-contraction coupling) in the ventricular cell as well as what is known for other cardiac cell types. Second, we review the molecular nature of the proteins that are involved in this process as well as the functional consequences of both normal and abnormal Ca 2+cycling (e.g., Ca 2+waves). Finally, we review what we understand to be the role of Ca 2+cycling in various forms of arrhythmias, that is, those associated with inherited mutations and those that are acquired and resulting from reentrant excitation and/or abnormal impulse generation (e.g., triggered activity). Further solving the nature of these intricate and dynamic interactions promises to be an important area of research for a better recognition and understanding of the nature of Ca 2+and arrhythmias. Our solutions will provide a more complete understanding of the molecular basis for the targeted control of cellular calcium in the treatment and prevention of such.
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Metadata
- Authors
- ter Keurs, H. E. D. J., & Boyden, P. A.
- Venue
- Physiological Reviews
- Publisher
- American Physiological Society
- Published
- 2007-04
- Volume
- 87
- Issue
- 2
- Pages
- 457-506
- ISSN
- 0031-9333 (ISSN-L)
- 1522-1210
- OpenAlex
- W2123374731
- Cited by
- 356
- References
- 441
- FWCI
- 4.19
- Type
- journal article
- Language
- en
- Open access
- green
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