Ca plays a crucial role in excitation-contraction coupling in cardiac myocytes. Dysfunctional Ca regulation alters the force of contraction and causes cardiac arrhythmias. Ca entry into cardiomyocytes is mediated mainly through L-type Ca channels, leading to the subsequent Ca release from the sarcoplasmic reticulum. L-type Ca channels are composed of the conventional Ca1.2, ubiquitously expressed in all heart chambers, and the developmentally regulated Ca1.3, exclusively expressed in the atria, sinoatrial node, and atrioventricular node in the adult heart. As such, Ca1.3 is implicated in the pathogenesis of sinoatrial and atrioventricular node dysfunction as well as atrial fibrillation. More recently, Ca1.3 expression was suggested in heart failure. Here, we review the functional role, expression levels, and regulation of Ca1.3 in the heart, including in the context of cardiac diseases. We believe that the elucidation of the functional and molecular pathways regulating Ca1.3 in the heart will assist in developing novel targeted therapeutic interventions for the aforementioned arrhythmias.
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| http://dx.doi.org/10.3389/fphys.2023.1144069 | DOI Listing |
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