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Cardiac-targeted expression of truncated K(v)4.2 subunit (K(v)4.2N) reduces transient outward current (I(to)) density, prolongs action potentials (APs), and enhances contractility in 3- to 4-week-old transgenic mice. By 13 to 15 weeks of age, these mice develop severely impaired cardiac function and signs of heart failure. In this study, we examined whether augmented contractility in K(v)4.2N mice results from elevations in intracellular calcium ([Ca2+]i) secondary to AP prolongation and investigated the putative roles of calcineurin activation in heart disease development of K(v)4.2N mice.

circulation

Inhibition of Calcineurin and Sarcolemmal Ca <sup>2+</sup> Influx Protects Cardiac Morphology and Ventricular Function in K <sub>v</sub> 4.2N Transgenic Mice

Inhibition of Calcineurin and Sarcolemmal Ca 2+ Influx Protects Cardiac Morphology and Ventricular Function in K v 4.2N Transgenic Mice

Inhibition of Calcineurin and Sarcolemmal Ca ²⁺ Influx Protects Cardiac Morphology and Ventricular Function in K _v 4.2N Transgenic Mice