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首页> 外文期刊>American Journal of Physiology >The molecular basis of skeletal muscle atrophy.
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The molecular basis of skeletal muscle atrophy.

机译：骨骼肌萎缩症的分子基础。

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摘要

Skeletal muscle atrophy attributable to muscular inactivity has significant adverse functional consequences. While the initiating physiological event leading to atrophy seems to be the loss of muscle tension and a good deal of the physiology of muscle atrophy has been characterized, little is known about the triggers or the molecular signaling events underlying this process. Decreases in protein synthesis and increases in protein degradation both have been shown to contribute to muscle protein loss due to disuse, and recent work has delineated elements of both synthetic and proteolytic processes underlying muscle atrophy. It is also becoming evident that interactions among known proteolytic pathways (ubiquitin-proteasome, lysosomal, and calpain) are involved in muscle proteolysis during atrophy. Factors such as TNF-alpha, glucocorticoids, myostatin, and reactive oxygen species can induce muscle protein loss under specified conditions. Also, it is now apparent that the transcription factor NF-kappaB is a key intracellular signal transducer in disuse atrophy. Transcriptional profiles of atrophying muscle show both up- and downregulation of various genes over time, thus providing further evidence that there are multiple concurrent processes involved in muscle atrophy. The purpose of this review is to synthesize our current understanding of the molecular regulation of muscle atrophy. We also discuss how ongoing work should uncover more about the molecular underpinnings of muscle wasting, particularly that due to disuse.
机译：归因于肌肉不活动的骨骼肌萎缩具有明显的不良功能后果。虽然导致萎缩的起始生理事件似乎是肌肉张力的丧失，并且已经表征了许多肌肉萎缩的生理学，但对于引起该过程的触发因素或分子信号事件知之甚少。蛋白质合成的减少和蛋白质降解的增加均已显示出由于废弃而导致肌肉蛋白质损失的原因，最近的工作描述了肌肉萎缩背后的合成和蛋白水解过程的要素。越来越明显的是，已知蛋白水解途径（遍在蛋白-蛋白酶体，溶酶体和钙蛋白酶）之间的相互作用与萎缩过程中的肌肉蛋白水解有关。在特定条件下，诸如TNF-α，糖皮质激素，肌生长抑制素和活性氧等因子可导致肌肉蛋白质损失。同样，现在很明显，转录因子NF-κB是废用萎缩的关键细胞内信号转导子。萎缩性肌肉的转录谱显示随着时间的推移各种基因的上调和下调，因此提供了进一步的证据表明肌肉萎缩涉及多个同时发生的过程。这篇综述的目的是综合我们目前对肌肉萎缩的分子调控的理解。我们还将讨论正在进行的工作如何揭示更多关于肌肉消瘦的分子基础，尤其是由于废止所致。

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