Circadian rhythms, the molecular clock, and skeletal muscle.
Circadian rhythms, the molecular clock, and skeletal muscle.
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DOI：
10.1016/b978-0-12-385940-2.00009-7
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发表时间：
2011
影响因子：
--
通讯作者：
Esser KA
中科院分区：
文献类型：
--
作者：
Lefta M;Wolff G;Esser KA
从单细胞细菌到人类，几乎所有的生物体都表现出各种各样的行为、生理和生化节律。在哺乳动物中，昼夜节律控制着24小时内许多生理过程的时间，包括睡眠-觉醒周期、体温、进食和激素产生。这一研究主体已经导致了基于周期长度、相位和振幅的昼夜节律的定义特征。基本的昼夜节律行为是在大多数（如果不是全部）细胞类型（包括骨骼肌）中发现的分子时钟机制。哺乳动物的分子钟是一个复杂的多振荡网络，通过转录机制，定时蛋白质周转和小分子的输入进行调节。目前，对骨骼肌功能/代谢的昼夜节律方面知之甚少，但在理解骨骼肌中的分子钟方面取得了一些进展。本章的目的是提供基本的术语和昼夜节律的概念，更详细地回顾了分子钟的知识现状，并参考了骨骼肌中已知的内容。研究表明，分子钟在骨骼肌中是活跃的，肌肉特异性转录因子MyoD是分子钟的直接靶点。生物钟受损小鼠（Bmal 1 −/−和ClockΔ19小鼠）的骨骼肌很弱，并且在成人肌肉结构和代谢所需的许多基因的表达中表现出显着的破坏。我们认为，分子时钟，MyoD和代谢因子，如PGC-1之间的相互作用，提供了一个潜在的反馈回路系统，可能是至关重要的维持和适应骨骼肌。
Almost all organisms ranging from single cell bacteria to humans exhibit a variety of behavioral, physiological, and biochemical rhythms. In mammals, circadian rhythms control the timing of many physiological processes over a 24-h period, including sleep-wake cycles, body temperature, feeding, and hormone production. This body of research has led to defined characteristics of circadian rhythms based on period length, phase, and amplitude. Underlying circadian behaviors is a molecular clock mechanism found in most, if not all, cell types including skeletal muscle. The mammalian molecular clock is a complex of multiple oscillating networks that are regulated through transcriptional mechanisms, timed protein turnover, and input from small molecules. At this time, very little is known about circadian aspects of skeletal muscle function/metabolism but some progress has been made on understanding the molecular clock in skeletal muscle. The goal of this chapter is to provide the basic terminology and concepts of circadian rhythms with a more detailed review of the current state of knowledge of the molecular clock, with reference to what is known in skeletal muscle. Research has demonstrated that the molecular clock is active in skeletal muscles and that the muscle-specific transcription factor, MyoD, is a direct target of the molecular clock. Skeletal muscle of clock-compromised mice, Bmal1−/− and ClockΔ19 mice, are weak and exhibit significant disruptions in expression of many genes required for adult muscle structure and metabolism. We suggest that the interaction between the molecular clock, MyoD, and metabolic factors, such as PGC-1, provide a potential system of feedback loops that may be critical for both maintenance and adaptation of skeletal muscle.