Why the study?
Pathways that negatively regulate the CaMKII/Nav1.5 axis were unknown and essential for designing new therapies to regulate pathogenic late sodium current associated with fatal arrhythmias.
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Population
B56α KO mice and myocytes
Comparison
B56α knockout vs control or adrenergic stimulation conditions
Design
In vivo and in vitro animal experimental and computational modeling study
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Hypothesis-generating for I_Na,L-targeted antiarrhythmics; leaves open translation from animal models to patients.
Refaey et al. (2019) studied this question.
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