Cav1.3 L-type calcium channels play a crucial role in cardiac pacemaking and atrioventricular conduction, and their dysfunction is implicated in sinoatrial node dysfunction, atrial fibrillation, and heart failure.
Ca 2+ plays a crucial role in excitation-contraction coupling in cardiac myocytes. Dysfunctional Ca 2+ regulation alters the force of contraction and causes cardiac arrhythmias. Ca 2+ entry into cardiomyocytes is mediated mainly through L-type Ca 2+ channels, leading to the subsequent Ca 2+ release from the sarcoplasmic reticulum. L-type Ca 2+ channels are composed of the conventional Ca v 1.2, ubiquitously expressed in all heart chambers, and the developmentally regulated Ca v 1.3, exclusively expressed in the atria, sinoatrial node, and atrioventricular node in the adult heart. As such, Ca v 1.3 is implicated in the pathogenesis of sinoatrial and atrioventricular node dysfunction as well as atrial fibrillation. More recently, Ca v 1.3 de novo expression was suggested in heart failure. Here, we review the functional role, expression levels, and regulation of Ca v 1.3 in the heart, including in the context of cardiac diseases. We believe that the elucidation of the functional and molecular pathways regulating Ca v 1.3 in the heart will assist in developing novel targeted therapeutic interventions for the aforementioned arrhythmias.
Zaveri et al. (Tue,) conducted a review in Cardiac arrhythmias and heart failure. Cav1.3 L-type calcium channels was evaluated. Cav1.3 L-type calcium channels play a crucial role in cardiac pacemaking and atrioventricular conduction, and their dysfunction is implicated in sinoatrial node dysfunction, atrial fibrillation, and heart failure.
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