Oxidative stress and sarcomeric proteins.
Oxidative stress and sarcomeric proteins.
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DOI：
10.1161/circresaha.111.300496
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发表时间：
2013-01-18
影响因子：
20.1
通讯作者：
Steinberg SF
中科院分区：
文献类型：
--
作者：
Steinberg SF
氧化应激伴随着广泛的临床上重要的心脏疾病，包括缺血/再灌注、糖尿病和高血压性心脏病。虽然活性氧（ROS）可以激活有助于缺血预处理和心脏保护的信号通路，但高水平的ROS诱导肌节的结构修饰，从而影响泵功能和心力衰竭的发病机制。然而，收缩性的氧化还原依赖性变化的确切性质是由氧化剂种类的来源/身份、氧化应激的水平和肌节内单个蛋白质上氧化剂诱导的翻译后修饰的化学/位置决定的。本文综述了ROS诱导的肌丝蛋白的各种翻译后修饰（包括肌丝蛋白的直接氧化修饰、ROS激活的信号酶引起的肌丝蛋白磷酸化和ROS激活的蛋白酶引起的肌丝蛋白裂解），这些修饰与心肌收缩力的控制有关。
Oxidative stress accompanies a wide spectrum of clinically important cardiac disorders, including ischemia/reperfusion, diabetes, and hypertensive heart disease. While reactive oxygen species (ROS) can activate signaling pathways that contribute to ischemic preconditioning and cardioprotection, high levels of ROS induce structural modifications of the sarcomere that impact on pump function and the pathogenesis of heart failure. However, the precise nature of the redox-dependent change in contractility is determined by the source/identity of the oxidant species, the level of oxidative stress, and the chemistry/position of oxidant-induced post-translational modifications on individual proteins within the sarcomere. This review focuses on various ROS-induced post-translational modifications of myofilament proteins (including direct oxidative modifications of myofilament proteins, myofilament protein phosphorylation by ROS-activated signaling enzymes, and myofilament protein cleavage by ROS-activated proteases) that have been implicated in the control of cardiac contractility.