Key result
JTV519, a 1,4-benzothiazepine derivative, increased the affinity of calstabin2 for RyR2, stabilizing its closed state and preventing the intracellular calcium leak that triggers fatal arrhythmias.
Why the study?
Does JTV519 prevent arrhythmogenic Ca2+ leak in models of heart failure and sudden cardiac death?
Population
Animal models of heart failure and cellular models of inherited forms of exercise-induced sudden cardiac death
Design
Preclinical
Authors
Loading...
JTV519 stabilizes RyR2 in animal models; hypothesis-generating for arrhythmia prevention in heart failure, with no clinical implications yet.
Does JTV519 prevent arrhythmogenic Ca2+ leak in models of heart failure and sudden cardiac death?
Enhancing the binding of calstabin2 to RyR2 with JTV519 prevents arrhythmogenic calcium leak, representing a potential novel therapeutic strategy for ventricular arrhythmias.
Wehrens et al. (2004) studied Ventricular arrhythmias. JTV519 (1,4-benzothiazepine derivative) was evaluated on Prevention of intracellular Ca2+ leak and stabilization of RyR2. JTV519, a 1,4-benzothiazepine derivative, increased the affinity of calstabin2 for RyR2, stabilizing its closed state and preventing the intracellular calcium leak that triggers fatal arrhythmias.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: