CaMKII oxidative activation and the pathogenesis of cardiac disease.
CaMKII oxidative activation and the pathogenesis of cardiac disease.
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DOI：
10.1016/j.yjmcc.2014.02.004
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发表时间：
2014-08
影响因子：
5
通讯作者：
Anderson, Mark E.
中科院分区：
文献类型：
--
作者：
Luczak, Elizabeth D.;Anderson, Mark E.
关键词：
钙离子和氧化还原信号在心脏疾病的发病机制中都起着重要作用;尽管这些信号如何在心脏中整合仍不清楚。心脏中钙和氧化应激的一个假定传感器是CaMKII，这是一种钙激活的激酶，最近已被证明也受氧化调节。CaMKII的氧化激活发生在几种心脏病模型中，包括心肌损伤和炎症、过度神经体液激活、心房颤动和窦房结功能障碍。此外，CaMKII的氧化活化在钙和ROS信号交叉的亚细胞结构域中，如线粒体。本文综述了氧化激活CAMKII的机制，氧化的CaMKII已被确定的心脏疾病，并提出氧化的CaMKII可能发挥重要作用的背景。
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.
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DOI：
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发表时间：
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影响因子：
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