Key result
Incremental elevation of luminal Ca2+ increased the probability of opening to 0.3-0.4 for CPVT mutant RyR2 versus 0.02 for wild-type RyR2, supporting a unifying theory of SOICR for CPVT and MH.
This paper proposes a unifying mechanistic model wherein CPVT and malignant hyperthermia are both triggered by a lowered threshold for store overload-induced Ca2+ release (SOICR) resulting from RYR or CASQ mutations.
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May inform SOICR-targeted therapies in CPVT and MH; leaves open clinical translation from cell models.
MacLennan et al. (2009) conducted a review in Catecholaminergic polymorphic ventricular tachycardia (CPVT) and Malignant hyperthermia (MH). Incremental elevation of luminal Ca2+ increased the probability of opening to 0.3-0.4 for CPVT mutant RyR2 versus 0.02 for wild-type RyR2, supporting a unifying theory of SOICR for CPVT and MH.
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