Population
Heterozygous cardiac calsequestrin-deficient mice (Casq2+/-) (n=35) and wild-type mice (Casq2+/+) (n=31)
Comparison
Isoproterenol challenge and programmed stimulation vs Wild-type mice (Casq2+/+)
Design
Preclinical
Authors
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Casq2 loss promotes catecholaminergic arrhythmias via leak despite SR adaptations in mice; leaves open direct versus indirect regulation in human CPVT.
Modest reductions in cardiac calsequestrin directly increase SR Ca2+ leak and susceptibility to ventricular tachycardia under stress, independent of luminal Ca2+ buffering.
Chopra et al. (2007) studied this question.
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