Key result
Calmodulin and CaMKII act as important modulators of cardiac ion channels, participating in feedback modulation to control electrical activity.
Provides a review of the mechanisms by which CaM and CaMKII regulate cardiac ion channels, including a novel model for Ca(V)1.2 regulation.
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Highlights CaM/CaMKII feedback in cardiac excitability; leaves open whether targeting these pathways improves arrhythmia outcomes.
Because changes in intracellular Ca(2+) concentration are the final signals of electrical activity in excitable cells, many mechanisms have evolved to regulate Ca(2+) influx. Among the most important are those pathways that directly regulate the ion channels responsible for regulating and generating the Ca(2+) influx signal. Recent work has demonstrated that the Ca(2+) binding protein calmodulin (CaM) and the Ca(2+)/CaM-sensitive kinase CaMKII are important modulators of cardiac ion channels. Thus, Ca(2+) participates in feedback modulation to control electrical activity. This review highlights various mechanisms by which CaM and CaMKII regulate cardiovascular ion channel activity and presents a novel model for CaMKII regulation of Ca(V)1.2 Ca(2+) channel function.
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Geoffrey S. Pitt (2006) conducted a review in Cardiac ion channel regulation. Calmodulin and CaMKII was evaluated. Calmodulin and CaMKII act as important modulators of cardiac ion channels, participating in feedback modulation to control electrical activity.
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