June 15, 2013AJP Heart and Circulatory Physiology
Post-translational modifications of the cardiac Na channel: contribution of CaMKII-dependent phosphorylation to acquired arrhythmias
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Key result
CaMKII-dependent phosphorylation of the cardiac Na channel alters channel gating, leading to both gain- and loss-of-function effects that contribute to acquired arrhythmias in heart failure.
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Implication
Supports CaMKII-NaV1.5 interactions in HF arrhythmias; leaves open targeted therapies pending prospective validation.
PICO
P
Population
Cardiac arrhythmias and heart failure
E
Exposure / Comparator
CaMKII-dependent phosphorylation
Post-translational modifications of the cardiac sodium channel NaV1.5, particularly by CaMKII, play a crucial role in altering channel function and promoting arrhythmogenesis in acquired cardiac disorders such as heart failure.
Cite This Study
Herren et al. (2013) conducted a review in Cardiac arrhythmias and heart failure. CaMKII-dependent phosphorylation was evaluated. CaMKII-dependent phosphorylation of the cardiac Na channel alters channel gating, leading to both gain- and loss-of-function effects that contribute to acquired arrhythmias in heart failure.
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