Abstract
It has been recognized for some time that intracellular Ca2+ ([Ca2+]i) can contribute to the genesis of cardiac arrhythmias, but understanding of the molecular signaling machinery that links disordered [Ca2+]i to arrhythmias has been lacking. Exciting recent work has focused on the ubiquitous intracellular Ca2+-binding protein calmodulin. Calmodulin is a molecular sensor that can translate increases in [Ca2+]i into modulatory signals for ion channels and activate other Ca2+-dependent signaling molecules. This article will examine the implications of these recent findings for arrhythmogenesis and the development of new antiarrhythmic therapies.
Original language | English (US) |
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Pages (from-to) | 195-197 |
Number of pages | 3 |
Journal | Journal of cardiovascular electrophysiology |
Volume | 13 |
Issue number | 2 |
DOIs | |
State | Published - 2002 |
Externally published | Yes |
Keywords
- Afterdepolarizations
- Calmodulin kinase
- Cardiomyopathy
- L-type calcium current
- Transient inward current
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Physiology (medical)