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首页> 外文期刊>Journal of Cellular Physiology >The Role of Exercise and TFAM in Preventing Skeletal Muscle Atrophy
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The Role of Exercise and TFAM in Preventing Skeletal Muscle Atrophy

机译:锻炼和TFAM预防的作用骨骼肌萎缩

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Skeletal muscle atrophy is the consequence of protein degradation exceeding protein synthesis. This arises for a multitude of reasons including the unloading of muscle during microgravity, post-surgery bedrest, immobilization of a limb after injury, and overall disuse of the musculature. The development of therapies prior to skeletal muscle atrophy settings to diminish protein degradation is scarce. Mitochondrial dysfunction is associated with skeletal muscle atrophy and contributes to the induction of protein degradation and cell apoptosis through increased levels of ROS observed with the loss of organelle function. ROS binds mtDNA, leading to its degradation and decreasing functionality. Mitochondrial transcription factor A (TFAM) will bind and coat mtDNA, protecting it from ROS and degradation while increasing mitochondrial function. Exercise stimulates cell signaling pathways that converge on and increase PGC-1 alpha, a well-known activator of the transcription of TFAM and mitochondrial biogenesis. Therefore, in the present review we are proposing, separately, exercise and TFAM treatments prior to atrophic settings (muscle unloading or disuse) alleviate skeletal muscle atrophy through enhanced mitochondrial adaptations and function. Additionally, we hypothesize the combination of exercise and TFAM leads to a synergistic effect in targeting mitochondrial function to prevent skeletal muscle atrophy. (C) 2016 The Authors. Journal of Cellular Physiology Published by Wiley Periodicals, Inc.
机译:骨骼肌萎缩的结果蛋白质降解超过蛋白质合成。这对众多的原因包括出现肌肉在微重力的卸货,对象床支架,固定的肢体受伤后,整体停止使用肌肉组织。减少骨骼肌萎缩设置蛋白质降解是稀缺的。与骨骼肌功能障碍有关萎缩和导致的感应蛋白质降解和细胞凋亡ROS水平上升的损失细胞器的功能。其退化和减少功能。线粒体转录因子(TFAM)绑定和外套mtDNA,从ROS和保护它退化,同时增加线粒体函数。途径和增加PGC-1收敛α,一位知名的活化剂转录TFAM和线粒体生物转化。建议,另外,锻炼和TFAM吗治疗前(肌肉萎缩性设置卸载或停止使用)减轻骨骼肌通过增强线粒体萎缩适应和功能。假定运动和TFAM的结合导致目标的协同效应防止骨骼肌线粒体功能萎缩。细胞生理由威利出版期刊、公司。

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