Why the study?
Does IP3R2 deficiency prevent endothelin-1-induced arrhythmogenic Ca2+ signaling in atrial myocytes?
Population
IP3R2-deficient mice and wild-type (WT) mice (atrial myocytes)
Comparison
Endothelin-1 (ET-1) stimulation vs Wild-type atrial myocytes vs IP3R2-deficient…
Design
Preclinical
Authors
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IP3R2 deficiency may block ET-1 arrhythmogenic Ca2+ release in atria; leaves open therapeutic targeting in human AF.
Does IP3R2 deficiency prevent endothelin-1-induced arrhythmogenic Ca2+ signaling in atrial myocytes?
Lack of IP3R2 abolishes the positive inotropic effect of neurohumoral stimulation with ET-1 and protects from its arrhythmogenic effects in atrial myocytes.
Li et al. (2005) studied this question.
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