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CaMKII Phosphorylation of NaV1.5 is Pro-Arrhythmogenic. Arrhythmogenic mechanism of CaMKII based regulation of INa, showing different CaMKII based alterations in cardiac ion channel targets and contributions. The emphasis is on CaMKII sites on NaV1.5 at S571, S516, and T594 on the DI–II loop of NaV1.5. When loss- and gain-of-function effects combine with other CaMKII ion channel targets, this can further enhance ventricular arrhythmias and sudden cardiac death.
