Key result
CaMKII activation is linked to apoptosis, hypertrophy, and arrhythmia, while its pharmacological or genetic inhibition improves health outcomes in animal models.
CaMKII plays a significant role in cardiac arrhythmia, structural heart disease, and sudden death, highlighting its potential as a therapeutic target.
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Animal data link CaMKII to arrhythmia and remodeling; leaves open clinical translation of inhibition.
Calcium/calmodulin-dependent kinase II (CaMKII) is a multifunctional serine/threonine kinase widely distributed in a number of tissue types. Activation of CaMKII has been linked to important downstream physiological processes, including apoptosis, hypertrophy, and arrhythmia in the heart. Pharmacological or genetic inhibition of CaMKII has been shown to improve health outcomes in a number of animal models. In this review, we summarize the structural and functional properties of CaMKII and detail its role in cardiac arrhythmia, structural heart disease, and sudden death.
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Erickson et al. (2008) conducted a review in Cardiac arrhythmia. CaMKII was evaluated. CaMKII activation is linked to apoptosis, hypertrophy, and arrhythmia, while its pharmacological or genetic inhibition improves health outcomes in animal models.
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