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The ryanodine receptor channel as a molecular motif in atrial fibrillation: pathophysiological and therapeutic implications

Dobromir Dobrev, Niels Voigt, Xander H.T. Wehrens
DOI: http://dx.doi.org/10.1093/cvr/cvq324 734-743 First published online: 13 October 2010

Abstract

Atrial fibrillation (AF) is the most common cardiac arrhythmia and is associated with substantial morbidity and mortality. It causes profound changes in sarcoplasmic reticulum (SR) Ca2+ homeostasis, including ryanodine receptor channel dysfunction and diastolic SR Ca2+ leak, which might contribute to both decreased contractile function and increased propensity to atrial arrhythmias. In this review, we will focus on the molecular basis of ryanodine receptor channel dysfunction and enhanced diastolic SR Ca2+ leak in AF. The potential relevance of increased incidence of spontaneous SR Ca2+ release for both AF induction and/or maintenance and the development of novel mechanism-based therapeutic approaches will be discussed.

  • Calcium handling
  • Atrial fibrillation
  • Remodelling
  • Ryanodine
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