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Cardiovascular Research 2006 70(3):407-409; doi:10.1016/j.cardiores.2006.04.007
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Copyright © 2006, European Society of Cardiology

Unzipping RyR2 in adult cardiomyocytes: Getting closer to mechanisms of inherited ventricular arrhythmias?

Maria Fernandez-Velasco, Ana Maria Gomez and Sylvain Richard*

Physiopathologie Cardiovasculaire, INSERM, U-637, Université Montpellier1, CHU Arnaud de Villeneuve 34295 Montpellier Cedex 5, France

* Corresponding author. Tel.: +33 467 41 52 41; fax: +33 467 41 52 42. Email address: srichard@montp.inserm.fr

Received 4 April 2006; accepted 6 April 2006

The first 10% of the full text of this article appears below.

See article by Yang et al. [19] (pages 475–485) in this issue.

Malignant ventricular arrhythmias (VA) are a major cause of mortality and morbidity worldwide. Causative mechanisms are multiple and complex. VA can be generated by abnormal or instable repolarization of the action potential (AP) in myocytes. Perverted repolarization results mainly from congenital channelopathies, acquired diseases, including hypertrophy and heart failure (HF), or therapeutic intervention. Inherited arrhythmias are due to mutations, mostly in transmembrane ionic channels (Na+, K+, Ca2+) [1,2]. However, because Ca2+ regulates several ionic currents involved in AP repolarization [3], it was not counterintuitive to find that mutations in proteins regulating intracellular Ca2+ homeostasis . . . [Full Text of this Article]


   1. Mechanisms involved in RyR2-linked arrhythmias
 

   2. Effect of DPc10 in permeabilized ventricular myocytes
 

   3. Perspectives
 

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