Key result
T-type calcium channels (Cav3.1 and Cav3.2) are induced in the myocardium during disease and injury, and are putatively associated with calcium-dependent signaling pathways in cardiac hypertrophy.
This review highlights the role and regulation of T-type calcium channels (Cav3.1 and Cav3.2) in the pathogenesis of cardiac disease and hypertrophy.
Leaves open whether T-type channel inhibition alters hypertrophy progression; warrants prospective interventional trials before clinical consideration.
The regulation of intracellular Ca (2+) is essential for cardiomyocyte function, and alterations in proteins that regulate Ca (2+) influx have dire consequences in the diseased heart. Low voltage-activated, T-type Ca (2+) channels are one pathway of Ca (2+) entry that is regulated according to developmental stage and in pathological conditions in the adult heart. Cardiac T-type channels consist of two main types, Cav3.1 (α1G) and Cav3.2 (α1H), and both can be induced in the myocardium in disease and injury but still, relatively little is known about mechanisms for their regulation and their respective functions. This article integrates previous data establishing regulation of T-type Ca (2+) channels in animal models of cardiac disease, with recent data that begin to address the functional consequences of cardiac Cav3.1 and Cav3.2 Ca (2+) channel expression in the pathological setting. The putative association of T-type Ca (2+) channels with Ca (2+) dependent signaling pathways in the context of cardiac hypertrophy is also discussed.
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Leanne L. Cribbs (2010) conducted a review in Cardiac disease and hypertrophy. T-type calcium channels (Cav3.1 and Cav3.2) was evaluated. T-type calcium channels (Cav3.1 and Cav3.2) are induced in the myocardium during disease and injury, and are putatively associated with calcium-dependent signaling pathways in cardiac hypertrophy.
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