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• W2016439178 abstract "CASQ2 (cardiac calsequestrin) is commonly believed to serve as the SR (sarcoplasmic reticulum) luminal Ca2+ sensor. Ablation of CASQ2 promotes SCWs (spontaneous Ca2+ waves) and CPVT (catecholaminergic polymorphic ventricular tachycardia) upon stress but not at rest. How SCWs and CPVT are triggered by stress in the absence of the CASQ2-based luminal Ca2+ sensor is an important unresolved question. In the present study, we assessed the role of the newly identified RyR2 (ryanodine receptor 2)-resident luminal Ca2+ sensor in determining SCW propensity, CPVT susceptibility and cardiac hypertrophy in Casq2-KO (knockout) mice. We crossbred Casq2-KO mice with RyR2 mutant (E4872Q+/−) mice, which lack RyR2-resident SR luminal Ca2+ sensing, to generate animals with both deficiencies. Casq2+/− and Casq2−/− mice showed stress-induced VTs (ventricular tachyarrhythmias), whereas Casq2+/−/E4872Q+/− and Casq2−/−/E4872Q+/− mice displayed little or no stress-induced VTs. Confocal Ca2+ imaging revealed that Casq2−/− hearts frequently exhibited SCWs after extracellular Ca2+ elevation or adrenergic stimulation, whereas Casq2−/−/E4872Q+/− hearts had few or no SCWs under the same conditions. Cardiac hypertrophy developed and CPVT susceptibility increased with age in Casq2−/− mice, but not in Casq2−/−/E4872Q+/− mice. However, the amplitudes and dynamics of voltage-induced Ca2+ transients in Casq2−/− and Casq2−/−/E4872Q+/− hearts were not significantly different. Our results indicate that SCWs, CPVT and hypertrophy in Casq2-null cardiac muscle are governed by the RyR2-resident luminal Ca2+ sensor. This implies that defects in CASQ2-based lumi-nal Ca2+ sensing can be overridden by the RyR2-resident luminal Ca2+ sensor. This makes this RyR2-resident sensor a promising molecular target for the treatment of Ca2+-mediated arrhythmias." @default.
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• W2016439178 date "2014-06-13" @default.
• W2016439178 modified "2023-10-17" @default.
• W2016439178 title "The cardiac ryanodine receptor luminal Ca2+ sensor governs Ca2+ waves, ventricular tachyarrhythmias and cardiac hypertrophy in calsequestrin-null mice" @default.
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• W2016439178 doi "https://doi.org/10.1042/bj20140126" @default.
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