Oxidative stress and disuse muscle atrophy: cause or consequence?
Oxidative stress and disuse muscle atrophy: cause or consequence?
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DOI：
10.1097/mco.0b013e328352b4c2
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发表时间：
2012-05
影响因子：
3.1
通讯作者：
Judge AR
中科院分区：
文献类型：
--
作者：
Powers SK;Smuder AJ;Judge AR
这篇综述将讨论支持和反对活性氧（ROS）在失活诱导的骨骼肌萎缩的调节中发挥重要作用的证据。众所周知，长时间的骨骼肌不活动会导致肌纤维萎缩和肌肉力量产生减少。这种废用诱导的肌肉萎缩是由于蛋白质降解增加和蛋白质合成减少导致的肌肉蛋白质损失的结果。最近的研究表明，氧化应激可以影响细胞信号转导途径，调节肌肉蛋白质的分解和合成在长时间的废用。具体而言，在骨骼肌不活动期间，肌纤维中增加的ROS产生可以促进增加的蛋白质水解并且还抑制蛋白质合成是可行的。虽然已经确定氧化剂可以参与细胞中蛋白质周转的调节，但是对于废用性骨骼肌萎缩是否需要氧化应激仍然存在争议。尽管如此，基于新出现的证据，我们得出结论，增加ROS生产的骨骼肌显着贡献失活引起的肌肉萎缩。
This review will discuss the evidence both for and against the concept that reactive oxygen species (ROS) play an important role in the regulation of inactivity-induced skeletal muscle atrophy. It is well established that prolonged skeletal muscle inactivity causes muscle fiber atrophy and a decrease in muscle force production. This disuse-induced muscle atrophy is the consequence of a loss in muscle protein resulting from increased protein degradation and decreased protein synthesis. Recent studies suggest that oxidative stress can influence cell signaling pathways that regulate both muscle protein breakdown and synthesis during prolonged periods of disuse. Specifically, it is feasible that increased ROS production in muscle fibers can promote increased proteolysis and also depress protein synthesis during periods of skeletal muscle inactivity. Although it is established that oxidants can participate in the regulation of protein turnover in cells, there remains debate as to whether oxidative stress is required for disuse skeletal muscle atrophy. Nonetheless, based on emerging evidence we conclude that increased ROS production in skeletal muscles significantly contributes to inactivity-induced muscle atrophy.