TY - JOUR
T1 - CaMKII oxidative activation and the pathogenesis of cardiac disease
AU - Luczak, Elizabeth D.
AU - Anderson, Mark E.
N1 - Funding Information:
This work was funded in part by the US National Institutes of Health ( R01HL70250 , R01HL079031 , R01HL113001 , and R01HL096652 ) and a grant ( 08CVD01 ) from the Fondation Leducq as part of the Alliance for CaMKII Signaling in Heart.
PY - 2014/8
Y1 - 2014/8
N2 - Calcium and redox signaling both play important roles in the pathogenesis of cardiac disease; although how these signals are integrated in the heart remains unclear. One putative sensor for both calcium and oxidative stress in the heart is CaMKII, a calcium activated kinase that has recently been shown to also be regulated by oxidation. Oxidative activation of CaMKII occurs in several models of cardiac disease, including myocardial injury and inflammation, excessive neurohumoral activation, atrial fibrillation, and sinus node dysfunction. Additionally, oxidative activation of CaMKII is suggested in subcellular domains where calcium and ROS signaling intersect, such as mitochondria. This review describes the mechanism of activation of CaMKII by oxidation, the cardiac diseases where oxidized CaMKII has been identified, and suggests contexts where oxidized CaMKII is likely to play an important role. This article is part of a Special Issue entitled "Redox Signalling in the Cardiovascular System".
AB - Calcium and redox signaling both play important roles in the pathogenesis of cardiac disease; although how these signals are integrated in the heart remains unclear. One putative sensor for both calcium and oxidative stress in the heart is CaMKII, a calcium activated kinase that has recently been shown to also be regulated by oxidation. Oxidative activation of CaMKII occurs in several models of cardiac disease, including myocardial injury and inflammation, excessive neurohumoral activation, atrial fibrillation, and sinus node dysfunction. Additionally, oxidative activation of CaMKII is suggested in subcellular domains where calcium and ROS signaling intersect, such as mitochondria. This review describes the mechanism of activation of CaMKII by oxidation, the cardiac diseases where oxidized CaMKII has been identified, and suggests contexts where oxidized CaMKII is likely to play an important role. This article is part of a Special Issue entitled "Redox Signalling in the Cardiovascular System".
KW - Arrhythmia
KW - Calcium
KW - Heart failure
KW - Mitochondria
KW - Reactive oxygen species
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U2 - 10.1016/j.yjmcc.2014.02.004
DO - 10.1016/j.yjmcc.2014.02.004
M3 - Review article
C2 - 24530899
AN - SCOPUS:84901847600
SN - 0022-2828
VL - 73
SP - 112
EP - 116
JO - Journal of Molecular and Cellular Cardiology
JF - Journal of Molecular and Cellular Cardiology
ER -