Authors
Simon Sedej, Albrecht Schmidt, Marco Denegri, Stefanie Walther, Marinko Matovina, Georg Arnstein, Eva-Maria Gutschi, Isabella Windhager, Senka Ljubojević, Sara Negri, Frank R Heinzel, Egbert Bisping, Marc A Vos, Carlo Napolitano, Silvia G Priori, Jens Kockskämper, Burkert Pieske
Publication date
2014/4/22
Journal
Journal of the American College of Cardiology
Volume
63
Issue
15
Pages
1569-1579
Publisher
American College of Cardiology Foundation
Description
Objectives
This study sought to explore whether subclinical alterations of sarcoplasmic reticulum (SR) Ca2+ release through cardiac ryanodine receptors (RyR2) aggravate cardiac remodeling in mice carrying a human RyR2R4496C+/– gain-of-function mutation in response to pressure overload.
Background
RyR2 dysfunction causes increased diastolic SR Ca2+ release associated with arrhythmias and contractile dysfunction in inherited and acquired cardiac diseases, such as catecholaminergic polymorphic ventricular tachycardia and heart failure (HF).
Methods
Functional and structural properties of wild-type and catecholaminergic polymorphic ventricular tachycardia–associated RyR2R4496C+/– hearts were characterized under conditions of pressure overload induced by transverse aortic constriction (TAC).
Results
Wild-type and RyR2R4496C+/– hearts had comparable structural and functional properties at …
Scholar articles
S Sedej, A Schmidt, M Denegri, S Walther, M Matovina… - Journal of the American College of Cardiology, 2014