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骨骼肌的氧化还原调节

Redox regulation of skeletal muscle.

作者信息

Jackson Malcolm J

机构信息

School of Clinical Sciences, University of Liverpool, Liverpool, UK.

出版信息

IUBMB Life. 2008 Aug;60(8):497-501. doi: 10.1002/iub.72.

DOI:10.1002/iub.72
PMID:18629903
Abstract

The potential deleterious roles of "oxidative stress" have been studied in skeletal muscle for over 30 years, but recent studies have identified that reactive oxygen species and nitric oxide generated by skeletal muscle can exert regulatory roles in cell signalling processes. This "redox regulation" appears to depend upon the reversible oxidation of cysteine residues within key proteins with reversible gluathionylation and formation of protein disulphides potentially leading to changes in the activities of proteins such as enzymes, transcription factors or transporters. Control of this process is dependent upon the local redox environment pertaining at a subcellular level. This short review provides examples of redox-regulated physiological processes in skeletal muscle that include some activation of transcription factors and changes in gene expression that result from contractile activity and the modulation of force generation during sustained contractions. There is also increasing evidence that dysregulation of redox-sensitive processes plays a role in the loss of muscle mass and function that occurs during normal ageing and in the gross muscle degeneration in disorders such as the muscular dystrophies.

摘要

在骨骼肌中,“氧化应激”潜在的有害作用已被研究了30多年,但最近的研究发现,骨骼肌产生的活性氧和一氧化氮可在细胞信号传导过程中发挥调节作用。这种“氧化还原调节”似乎取决于关键蛋白中半胱氨酸残基的可逆氧化,伴随着可逆的谷胱甘肽化以及蛋白质二硫键的形成,这可能导致酶、转录因子或转运蛋白等蛋白质活性发生变化。这一过程的控制取决于亚细胞水平的局部氧化还原环境。这篇简短的综述提供了骨骼肌中氧化还原调节的生理过程的例子,包括一些转录因子的激活以及因收缩活动和持续收缩过程中力量产生的调节而导致的基因表达变化。越来越多的证据表明,氧化还原敏感过程的失调在正常衰老过程中发生的肌肉质量和功能丧失以及诸如肌肉萎缩症等疾病中的严重肌肉退化中起作用。

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