| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 3030601 | Trends in Cardiovascular Medicine | 2011 | 4 Pages |
Abstract
Ryanodine receptor (RyR2) dysfunction, which may result from a variety of mechanisms, has been implicated in the pathogenesis of cardiac arrhythmias and heart failure. In this review, we discuss the important role of Ca2+/calmodulin-dependent protein kinase II (CaMKII) in the regulation of RyR2-mediated Ca2+ release. In particular, we examine how pathological activation of CaMKII can lead to an increased risk of sudden arrhythmic death. Finally, we discuss how reduction of CaMKII-mediated RyR2 hyperactivity might reduce the risk of arrhythmias and may serve as a rationale for future pharmacotherapeutic approaches.
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Authors
Mark D. McCauley, Xander H.T. Wehrens,