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Cardiovascular Research Advance Access originally published online on August 14, 2007
Cardiovascular Research 2008 77(2):293-301; doi:10.1093/cvr/cvm004
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2007. For Permissions please e-mail: journals.permissions@oxfordjournals.org

Disruption of calcium homeostasis and arrhythmogenesis induced by mutations in the cardiac ryanodine receptor and calsequestrin

Nian Liu1 and Silvia G. Priori1,2,*

1 Molecular Cardiology, Fondazione Salvatore Maugeri, Via Maugeri 10/1-A, 27100 Pavia Italy
2 Department of Cardiology, University of Pavia, Pavia, Italy

* Corresponding author. Tel: +39 0382 592051; fax: +39 0382 592059. E-mail address: spriori{at}fsm.it

Development of cardiac arrhythmias in several degenerative cardiac disorders such as heart failure is precipitated by abnormalities in intracellular calcium regulation. Recently, the identification of mutations in proteins responsible for the control of intracellular calcium has been associated with an inherited arrhythmogenic syndrome called catecholaminergic polymorphic ventricular tachycardia (CPVT). Here, we review the current knowledge about the molecular pathophysiology of CPVT and we discuss some potentially innovative strategies for controlling calcium-handling abnormalities in CPVT that may provide novel therapeutic options for affected patients.

KEYWORDS Ventricular arrhythmias; SR (function); Sudden death; E-c coupling; Calcium (cellular)

Time for primary review: 21 days


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