Calmodulin kinase II regulates atrial myocyte late sodium current, calcium handling, and atrial arrhythmia.

ABSTRACT:

Background

Atrial fibrillation (AF) is the most common type of arrhythmia. Abnormal atrial myocyte Ca²⁺ handling promotes aberrant membrane excitability and remodeling that are important for atrial arrhythmogenesis. The sequence of molecular events leading to loss of normal atrial myocyte Ca²⁺ homeostasis is not established. Late Na⁺ current (I_Na,L) is increased in atrial myocytes from AF patients together with an increase in activity of Ca²⁺/calmodulin-dependent kinase II (CaMKII).

Objective

The purpose of this study was to determine whether CaMKII-dependent phosphorylation at Ser571 on Na_V1.5 increases atrial I_Na,L, leading to aberrant atrial Ca²⁺ cycling, altered electrophysiology, and

SUBMITTER: Greer-Short A 

PROVIDER: S-EPMC7056561 | biostudies-literature | 2020 Mar

REPOSITORIES: biostudies-literature