Cardiac FKBP12.6 overexpression protects against triggered ventricular tachycardia in pressure overloaded mouse hearts

Alterations in RyR2 function have been proposed as a major pathophysiological mechanism of arrhythmias and heart failure (HF). Cardiac FKBP12.6 overexpression protects against myocardial infarction-induced HF and catecholamine-promoted ventricular arrhythmias. We tested the hypothesis that FKBP12.6...

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Veröffentlicht in:	Basic research in cardiology 2012-03, Vol.107 (2), p.246-246, Article 246
Hauptverfasser:	Vinet, Laurent, Pezet, Mylène, Bito, Virginie, Briec, François, Biesmans, Liesbeth, Rouet-Benzineb, Patricia, Gellen, Barnabas, Prévilon, Miresta, Chimenti, Stefano, Vilaine, Jean-Paul, Charpentier, Flavien, Sipido, Karin R., Mercadier, Jean-Jacques
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Cardiology Electrocardiography Heart Failure - genetics Heart Failure - metabolism Heart Failure - physiopathology Immunoblotting Male Medicine Medicine & Public Health Mice Mice, Transgenic Myocardium - metabolism Myocardium - pathology Original Contribution Real-Time Polymerase Chain Reaction Reverse Transcriptase Polymerase Chain Reaction Tachycardia, Ventricular - genetics Tachycardia, Ventricular - metabolism Tachycardia, Ventricular - physiopathology Tacrolimus Binding Proteins - genetics Tacrolimus Binding Proteins - metabolism Up-Regulation Ventricular Remodeling - genetics
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Zusammenfassung:	Alterations in RyR2 function have been proposed as a major pathophysiological mechanism of arrhythmias and heart failure (HF). Cardiac FKBP12.6 overexpression protects against myocardial infarction-induced HF and catecholamine-promoted ventricular arrhythmias. We tested the hypothesis that FKBP12.6 overexpression protects against maladaptive LVH and triggered ventricular arrhythmias following transverse aorta constriction (TAC) in the mouse. The TAC-associated mortality rate was significantly lower in male transgenic (DT) than in Ctr mice ( p
ISSN:	0300-8428 1435-1803
DOI:	10.1007/s00395-012-0246-8