Understanding the mechanistic basis of RyR2 dysfunction is essential for developing novel therapies to prevent arrhythmia and sudden cardiac death in susceptible individuals.
RyR2 mutation insights advance preclinical therapy development; leaves open clinical translation for arrhythmia prevention.
Mutations in ryanodine receptor calcium ion-release channels (RyR2) have emerged as important causative players in exercise/stress-induced ventricular arrhythmia leading to sudden cardiac death (SCD). Thus, RyR2 represents an attractive therapeutic target, and a detailed understanding of the mechanistic basis of RyR2 dysfunction at the molecular, cellular and organ level is essential for the development of novel, more effective therapeutic approaches to prevent arrhythmia and SCD. Such advances will translate into a tremendous improvement in the survival and quality of life of SCD-susceptible individuals. In this review, the authors consider how recent knowledge gained from mutation identification, phenotypic manifestation and functional evaluation of RyR2 mutants, are being used to develop novel therapeutic strategies in RyR2-dependent arrhythmia.
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Thomas et al. (2005) studied this question.
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