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• W2079786003 abstract "The multifunctional Ca2+ and calmodulin-dependent protein kinase II (CaMKII) has emerged as an interesting proarrhythmic and procardiomyopathic signaling molecule with therapeutic potential. The importance of this growing body of evidence showing that CaMKII plays a central role in myocardial disease is evidenced, in part, by this thematic series dedicated to CaMKII. The first studies that CaMKII could participate in ion channel biology in heart were reported in 1994 when separate papers from the Anderson, Bers, and Lakatta groups identified CaMKII as a signal that was important for L-type Ca2+ current (ICa) facilitation. CaMKII induces L-type Ca2+ channels to enter a highly active gating mode, characterized by long and frequent openings, 1 Dzhura I. Wu Y. Colbran R.J. Balser J.R. Anderson M.E. Calmodulin kinase determines calcium-dependent facilitation of L-type calcium channels. Nat Cell Biol. 2000; 2: 173-177 Crossref PubMed Scopus (302) Google Scholar which can underlie arrhythmia-inducing afterdepolarizations. 2 Sun A.Y. Pitt G.S. Pinning down the CaMKII targets in the L-type Ca2+ channel: An essential step in defining CaMKII regulation. Heart Rhythm. 2011; 8: 631-633 Abstract Full Text Full Text PDF PubMed Scopus (7) Google Scholar I became interested in the potential for CaMKII to act as a proarrhythmic, feed-forward, signal to L-type Ca2+ channels when I was a trainee in cardiovascular medicine and electrophysiology at Stanford. I was fortunate to develop a collaboration with Howard Schulman, who discovered CaMKII when he was a postdoctoral fellow in the laboratory of Paul Greengard in 1978. 3 Schulman H. Greengard P. Stimulation of brain membrane protein phosphorylation by calcium and an endogenous heat-stable protein. Nature. 1978; 271: 478-479 Crossref PubMed Scopus (218) Google Scholar Initial investigations of CaMKII, particularly by neuroscientists, focused on the role of CaMKII in noncardiac tissue. However, in my opinion, the best understood role of CaMKII as a disease signal is in the cardiovascular system. Our group was the first to identify CaMKII as a proarrhythmic signaling molecule. 4 Anderson M.E. Braun A.P. Wu Y. Lu T. Schulman H. Sung R.J. KN-93, an inhibitor of multifunctional Ca++/calmodulin-dependent protein kinase, decreases early afterdepolarizations in rabbit heart. J Pharm Exp Ther. 1998; 287: 996-1006 PubMed Google Scholar However, since these early reports, work from many laboratories represented in this series and from others has shown that CaMKII promotes pathologic membrane excitability and hypertrophic transcription, activates cell death machinery, and disturbs intracellular Ca2+ homeostasis. The diversity of these processes sparked the realization that CaMKII acts as a master regulator of cellular processes that are intimately involved in heart failure and arrhythmias. It may be that the apparent vulnerability in the design of the CaMKII pathway is a natural consequence of the multiple downstream CaMKII targets and the core physiologic roles of CaMKII in myocardium. For example, by targeting sarcolemmal ion channels and intracellular Ca2+ homeostatic proteins, CaMKII is positioned to serve as a physiologic interface between membrane excitability and sarcoplasmic reticulum Ca2+ release, two processes that are essential for excitation–contraction coupling. 5 Wu Y. Colbran R.J. Anderson M.E. Calmodulin kinase is a molecular switch for cardiac excitation - contraction coupling. Proc Natl Acad Sci U S A. 2001; 98: 2877-2881 Crossref PubMed Scopus (77) Google Scholar However, this interface is also a hotspot for linking pathologic membrane excitability (i.e., arrhythmias) and contractile dysfunction (i.e., heart failure)." @default.
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• W2079786003 date "2011-09-01" @default.
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• W2079786003 title "Pathways for CaMKII activation in disease" @default.
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• W2079786003 doi "https://doi.org/10.1016/j.hrthm.2011.04.027" @default.
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