Mitochondrial Dysfunction and Oxidative Damage to Sarcomeric Proteins
Mitochondrial Dysfunction and Oxidative Damage to Sarcomeric Proteins
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DOI：
10.1007/s11906-010-0149-8
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发表时间：
2010-12-01
影响因子：
5.6
通讯作者：
Ardehali, Hossein
中科院分区：
文献类型：
--
作者：
Bayeva, Marina;Ardehali, Hossein
高血压是心力衰竭发展的重要危险因素。活性氧（ROS）的产生增加通过激活许多促肥大信号级联和损伤线粒体而导致心脏功能障碍，从而引发ROS产生的恶性循环。然而，氧化应激导致收缩和舒张功能障碍恶化的方式仍不清楚。在骨骼肌和缺血性心肌中，增加的ROS产生导致肌原纤维蛋白的优先氧化，并通过破坏肌动蛋白-肌球蛋白相互作用、酶功能、钙敏感性和跨桥循环效率，在氧化损伤和收缩性受损之间提供机制联系。在这篇综述中，我们总结了心力衰竭和肌节生物学领域的最新研究结果，并推测肌原纤维的氧化损伤可能有助于心力衰竭的发展。
Hypertension is an important risk factor for the development of heart failure. Increased production of reactive oxygen species (ROS) contributes to cardiac dysfunction by activating numerous pro-hypertrophic signaling cascades and damaging the mitochondria, thus setting off a vicious cycle of ROS generation. The way in which oxidative stress leads to exacerbation of systolic and diastolic dysfunction is still unclear, however. In skeletal muscle and ischemic myocardium, increased ROS production causes preferential oxidation of myofibrillar proteins and provides a mechanistic link between oxidative damage and impaired contractility through disruption of actin-myosin interactions, enzymatic functions, calcium sensitivity, and efficiency of cross-bridge cycling. In this review, we summarize recent findings in the fields of heart failure and sarcomere biology and speculate that oxidative damage to myofibrils may contribute to the development of heart failure.