Key result
The RyR2-P2328S mutation in murine hearts resulted in marked alterations in cellular Ca2+ homeostasis and arrhythmogenic properties resembling CPVT, with greater effects in homozygotes.
Why the study?
Does the RyR2-P2328S mutation alter cellular Ca2+ homeostasis and arrhythmogenic properties in murine hearts?
Does the RyR2-P2328S mutation alter cellular Ca2+ homeostasis and arrhythmogenic properties in murine hearts?
The RyR2-P2328S mutation causes CPVT-like arrhythmias and altered calcium homeostasis in mice, demonstrating a gene dosage effect.
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RyR2-P2328S mutation disrupts myocyte Ca2+ homeostasis in mice; leaves open its mechanistic contribution to human CPVT and need for targeted therapies.
Goddard et al. (2008) studied Catecholaminergic polymorphic ventricular tachycardia (CPVT). RyR2-P2328S mutation vs. Wild-type (WT) mice was evaluated on Cellular Ca2+ homeostasis and arrhythmogenic properties (nsVTs, sVTs). The RyR2-P2328S mutation in murine hearts resulted in marked alterations in cellular Ca2+ homeostasis and arrhythmogenic properties resembling CPVT, with greater effects in homozygotes.
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