Ryanodine receptor phosphorylation, calcium/calmodulin-dependent protein kinase II, and life-threatening ventricular arrhythmias.

Trends in Cardiovascular Medicine
Mark D McCauley, Xander H T Wehrens

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 Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) in the regulation of RyR2-mediated Ca(2+) 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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Citations

Oct 13, 2012·Heart Rhythm : the Official Journal of the Heart Rhythm Society·Sean DeGrandePeter J Mohler
Jun 19, 2013·Biochimica Et Biophysica Acta·Sameer AtherXander H T Wehrens
Nov 26, 2013·Seminars in Cardiothoracic and Vascular Anesthesia·Theresa Anne Gelzinis
Jun 10, 2017·Circulation Research·Andrew P LandstromXander H T Wehrens
Jan 10, 2014·Circulation·Dan M Roden, Björn C Knollmann
Aug 24, 2018·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·Andrew R EdnieEric S Bennett
Mar 10, 2015·American Journal of Physiology. Heart and Circulatory Physiology·Alicia MattiazziDonald M Bers
Jan 6, 2021·Pflügers Archiv : European journal of physiology·Satadru K LahiriXander H T Wehrens
Jun 25, 2021·Journal of Applied Physiology·Mohsin Haseeb, Paul D Thompson

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