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减少衰老骨骼肌氧化损伤的策略。

Strategies for reducing oxidative damage in ageing skeletal muscle.

机构信息

University of Liverpool, UK.

出版信息

Adv Drug Deliv Rev. 2009 Nov 30;61(14):1363-8. doi: 10.1016/j.addr.2009.07.018. Epub 2009 Sep 6.

DOI:10.1016/j.addr.2009.07.018
PMID:19737589
Abstract

It is recognised that reactive oxygen species (ROS) are both key regulators of cellular signalling and initiators of oxidative damage to DNA, lipids and proteins under different circumstances. Thus in skeletal muscle from animals and humans, studies indicate that ROS can potentially contribute to the pathophysiology of the age-related loss of skeletal muscle mass and function, while additionally acting as a key signal for contraction-induced adaptations in the tissue. The specific nature and sources of generation of the ROS contributing to these actions remain unknown, but the combination of physiological and pathological roles of ROS imply that interventions based on a simple suppression of ROS activities through use on non-specific antioxidants are unlikely to retard or improve the age-related declines in muscle mass and function. This review will briefly describe the background to this area and describe alternative strategies aimed at correcting specific redox-related changes in ageing muscle, such as the decline in oxidative signalling pathways, that may indicate rational interventions to help maintain muscle mass and function in the elderly.

摘要

人们认识到,活性氧(ROS)既是细胞信号的关键调节剂,也是在不同情况下导致 DNA、脂质和蛋白质氧化损伤的引发剂。因此,在动物和人类的骨骼肌中,研究表明 ROS 可能有助于与年龄相关的骨骼肌质量和功能丧失的病理生理学,同时作为组织中收缩诱导适应的关键信号。促成这些作用的 ROS 的特定性质和产生来源尚不清楚,但 ROS 的生理和病理作用的结合意味着,通过使用非特异性抗氧化剂简单抑制 ROS 活性的干预措施不太可能延缓或改善与年龄相关的肌肉质量和功能下降。本文将简要描述该领域的背景,并描述旨在纠正与衰老肌肉相关的特定氧化还原变化的替代策略,例如氧化信号通路的下降,这可能表明合理的干预措施有助于维持老年人的肌肉质量和功能。

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