Abstract
Voltage-gated calcium channels are the major pathway for Ca2+ influx to initiate the contraction of smooth and cardiac muscles. Alterations of calcium channel function have been implicated in multiple cardiovascular diseases, such as hypertension, atrial fibrillation, and long QT syndrome. Post-translational modifications do expand cardiovascular calcium channel structure and function to affect processes such as channel trafficking or polyubiquitination by two E3 ubiquitin ligases, Ret finger protein 2 (Rfp2) or murine double minute 2 protein (Mdm2). Additionally, biophysical property such as Ca2+-dependent inactivation (CDI) could be altered through binding of calmodulin, or channel activity could be modulated via S-nitrosylation by nitric oxide and phosphorylation by protein kinases or by interacting protein partners, such as galectin-1 and Rem. Understanding how cardiovascular calcium channel function is post-translationally remodeled under distinctive disease conditions will provide better information about calcium channel-related disease mechanisms and improve the development of more selective therapeutic agents for cardiovascular diseases.
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