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Exercise training prevents ventricular tachycardia in CPVT1 due to reduced CaMKII-dependent arrhythmogenic Ca2+ release

机译:运动训练可防止因CaMKII依赖性心律失常所致Ca2 +释放减少而导致CPVT1中的室性心动过速

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摘要

Catecholaminergic polymorphic ventricular tachycardia type 1 (CPVT1) is caused by mutations in the cardiac ryanodine receptor (RyR2) that lead to disrupted Ca2+ handling in cardiomyocytes and ventricular tachycardia. The aim of this study was to test whether exercise training could reduce the propensity for arrhythmias in mice with the CPVT1-causative missense mutation Ryr2-R2474S by restoring normal Ca2+ handling.
机译:儿茶酚胺能性多形性室性心动过速1型(CPVT1)是由心脏ryanodine受体(RyR2)的突变引起的,该突变导致心肌细胞和室性心动过速中Ca2 +处理的中断。这项研究的目的是测试运动训练是否可以通过恢复正常的Ca2 +处理来降低CPVT1致错义突变Ryr2-R2474S小鼠的心律失常倾向。

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