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June 15, 2004Circulation

Sudden Death in Familial Polymorphic Ventricular Tachycardia Associated With Calcium Release Channel (Ryanodine Receptor) Leak

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Why the study?

Does JTV519 normalize channel function in PKA-phosphorylated mutant RyR2 channels associated with FPVT?

Population

Mutant RyR2 channels associated with familial polymorphic ventricular tachycardia in Finnish families

Comparison

Protein kinase A phosphorylation and… vs Untreated mutant RyR2 channels

Design

Preclinical

Authors

SLStephan E. LehnartElectrophysiologyXWXander H.T. WehrensElectrophysiologyPLPäivi J. LaitinenColumbia University

Discussion

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Overview

JTV519 may target RyR2 dysfunction in FPVT models; hypothesis-generating and requires clinical trials before any practice change.

Structured PICO

Does JTV519 normalize channel function in PKA-phosphorylated mutant RyR2 channels associated with FPVT?

P
Population
Mutant RyR2 channels (P2328S, Q4201R, and V4653F) associated with familial polymorphic ventricular tachycardia (FPVT) in Finnish families
I
Intervention
Protein kinase A (PKA) phosphorylation (to simulate exercise) and experimental drug JTV519
C
Comparator
Untreated mutant RyR2 channels
O
Outcome
RyR2 channel function and calstabin2 (FKBP12.6) bindingsurrogate

The experimental drug JTV519 normalizes RyR2 channel function in FPVT mutations, highlighting a potential therapeutic target for preventing exercise-induced sudden cardiac death.

Cite This Study

Lehnart et al. (2004) studied this question.

synapsesocial.com/papers/6a20cb3fe3e6025b589a893ahttps://doi.org/10.1161/01.cir.0000132472.98675.ec
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