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氧化还原信号与心肌肌节。

Redox signaling and cardiac sarcomeres.

机构信息

Department of Physiology, Center for Muscle Biology, University of Kentucky, Lexington, Kentucky 40536, USA.

出版信息

J Biol Chem. 2011 Mar 25;286(12):9921-7. doi: 10.1074/jbc.R110.175489. Epub 2011 Jan 21.

Abstract

Oxidative stress is common in many clinically important cardiac disorders, including ischemia/reperfusion, diabetes, and hypertensive heart disease. Oxidative stress leads to derangements in pump function due to changes in the expression or function of proteins that regulate intracellular Ca(2+) homeostasis. There is growing evidence that the cardiodepressant actions of reactive oxygen species (ROS) also are attributable to ROS-dependent signaling events in the sarcomere. This minireview focuses on myofilament protein post-translational modifications induced by ROS or ROS-activated signaling enzymes that regulate cardiac contractility.

摘要

氧化应激在许多临床上重要的心脏疾病中很常见,包括缺血/再灌注、糖尿病和高血压性心脏病。氧化应激导致泵功能紊乱,原因是调节细胞内 Ca(2+)稳态的蛋白质的表达或功能发生变化。越来越多的证据表明,活性氧(ROS)的心脏抑制作用也归因于肌节中 ROS 依赖的信号事件。这篇迷你评论集中讨论了 ROS 或 ROS 激活的信号酶诱导的肌球蛋白蛋白翻译后修饰,这些修饰调节心脏收缩性。

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