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

Cardiovasc Res. 2011 Mar 1;89(4):734-43. doi: 10.1093/cvr/cvq324. Epub 2010 Oct 12.

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) Ca(2+) homeostasis, including ryanodine receptor channel dysfunction and diastolic SR Ca(2+) 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 Ca(2+) leak in AF. The potential relevance of increased incidence of spontaneous SR Ca(2+) release for both AF induction and/or maintenance and the development of novel mechanism-based therapeutic approaches will be discussed.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Atrial Fibrillation / etiology*
  • Atrial Fibrillation / metabolism
  • Atrial Fibrillation / therapy
  • Calcium / metabolism
  • Calcium Signaling
  • Heart Atria / metabolism
  • Humans
  • Ryanodine Receptor Calcium Release Channel / physiology*
  • Sarcoplasmic Reticulum / metabolism
  • Sodium-Calcium Exchanger / physiology

Substances

  • Ryanodine Receptor Calcium Release Channel
  • Sodium-Calcium Exchanger
  • sodium-calcium exchanger 1
  • Calcium