Junctional ectopic tachycardia caused by junctophilin-2 expression silencing is selectively sensitive to ryanodine receptor blockade
Q Yang, HJ Tadros, B Sun, MT Bidzimou… - Basic to Translational …, 2023 - jacc.org
Q Yang, HJ Tadros, B Sun, MT Bidzimou, JE Ezekian, F Li, A Ludwig, XHT Wehrens…
Basic to Translational Science, 2023•jacc.orgJunctional ectopic tachycardia (JET) is a potentially fatal cardiac arrhythmia. Hcn4: shJph2
mice serve as a model of nodal arrhythmias driven by ryanodine type 2 receptor (RyR2)–
mediated Ca2+ leak. EL20 is a small molecule that blocks RyR2 Ca2+ leak. In a novel in
vivo model of JET, Hcn4: shJph2 mice demonstrated rapid conversion of JET to sinus rhythm
with infusion of EL20. Primary atrioventricular nodal cells demonstrated increased Ca2+
transient oscillation frequency and increased RyR2-mediated stored Ca2+ leak which was …
mice serve as a model of nodal arrhythmias driven by ryanodine type 2 receptor (RyR2)–
mediated Ca2+ leak. EL20 is a small molecule that blocks RyR2 Ca2+ leak. In a novel in
vivo model of JET, Hcn4: shJph2 mice demonstrated rapid conversion of JET to sinus rhythm
with infusion of EL20. Primary atrioventricular nodal cells demonstrated increased Ca2+
transient oscillation frequency and increased RyR2-mediated stored Ca2+ leak which was …
Summary
Junctional ectopic tachycardia (JET) is a potentially fatal cardiac arrhythmia. Hcn4:shJph2 mice serve as a model of nodal arrhythmias driven by ryanodine type 2 receptor (RyR2)–mediated Ca2+ leak. EL20 is a small molecule that blocks RyR2 Ca2+ leak. In a novel in vivo model of JET, Hcn4:shJph2 mice demonstrated rapid conversion of JET to sinus rhythm with infusion of EL20. Primary atrioventricular nodal cells demonstrated increased Ca2+ transient oscillation frequency and increased RyR2-mediated stored Ca2+ leak which was normalized by EL20. EL20 was found to be rapidly degraded in mouse and human plasma, making it a potential novel therapy for JET.
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