Abstract

Calcium flowing through voltage-dependent calcium channels into cardiomyocytes mediates excitation–contraction coupling, controls action-potential duration and automaticity in nodal cells, and regulates gene expression. Proper surface targeting and basal and hormonal regulation of calcium channels are vital for normal cardiac physiology. In this review, we discuss the roles of voltage-gated calcium channels in the heart and the mechanisms by which these channels are regulated by physiological signaling pathways in health and disease.

Highlights

  • In the heart, calcium (Ca2+) entry through the voltage-gated Ca2+ channel initiates muscle excitation–contraction coupling

  • We will discuss mechanisms of Ca2+ handling in the heart and how dysfunctions of voltage-gated Ca2+ channels can lead to arrhythmias

  • Only long-lasting (L)- and transient (T)-type Ca2+ channels are expressed in cardiomyocytes.[1,2]

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Summary

Introduction

Calcium (Ca2+) entry through the voltage-gated Ca2+ channel initiates muscle excitation–contraction coupling. The influx of Ca2+ contributes to the plateau phase of the action potential, pacemaker activity in nodal cells, and the modulation of critical cellular processes including metabolism and gene expression. A Ca2+ influx via voltage-gated Ca2+ channels in the heart links membrane depolarization to cellular functions. We will discuss mechanisms of Ca2+ handling in the heart and how dysfunctions of voltage-gated Ca2+ channels can lead to arrhythmias. Ca2+ channels are modulated by voltage, Ca2+, posttranslational modifications, and protein–protein interactions, which will be reviewed. We will discuss existing pharmacological therapies that target voltage-gated Ca2+ channels

Structure and cellular electrophysiological function
Skeletal muscle
Posttranslational regulation of calcium channels
Findings
Conclusions
Full Text
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