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Ca 2+ /calmodulin-dependent protein kinase II (CaMKII)-dependent L-type calcium channel (LTCC) current (I Ca ) remodeling is an important contributor to the disruption of calcium homeostasis in heart failure (HF). We have reported that Kv4.3 proteins play an important role in delicate regulation of the membrane-associated CaMKII activity in ventricular myocytes. Here, we investigated the effect of in vivo Kv4.3 expression on I Ca in HF left ventricular (LV) myocytes.

Kv4.3 expression reverses ICa remodeling in ventricular myocytes of heart failure