Chan S M H, Selemidis S, Vlahos R
Centre for Respiratory Science and Health, School of Health and Biomedical Sciences, RMIT University, Melbourne, VIC 3001, Australia.
Antioxidants (Basel). 2024 Jul 22;13(7):882. doi: 10.3390/antiox13070882.
An elevation in reactive oxygen species (ROS) is widely accepted to be a key mechanism that drives chronic obstructive pulmonary disease (COPD) and its major co-morbidity, skeletal muscle wasting. However, it will be perhaps a surprise to many that an elevation in ROS in skeletal muscle is also a critical process for normal skeletal muscle function and in the adaptations to physical exercise. The key message here is that ROS are not solely detrimental. This duality of ROS suggests that the mere use of a broad-acting antioxidant is destined to fail in alleviating skeletal muscle wasting in COPD because it will also be influencing critical physiological ROS-dependent processes. Here, we take a close look at this duality of ROS in skeletal muscle physiology and pathophysiology pertaining to COPD and will aim to gain critical insights from other skeletal muscle wasting conditions due to aging such as sarcopenia.
活性氧(ROS)水平升高被广泛认为是驱动慢性阻塞性肺疾病(COPD)及其主要合并症骨骼肌萎缩的关键机制。然而,可能令许多人惊讶的是,骨骼肌中ROS水平升高对于正常骨骼肌功能以及对体育锻炼的适应性也是一个关键过程。这里的关键信息是,ROS并不只是有害的。ROS的这种双重性表明,仅仅使用一种作用广泛的抗氧化剂注定无法缓解COPD患者的骨骼肌萎缩,因为它也会影响关键的生理ROS依赖性过程。在这里,我们仔细研究ROS在与COPD相关的骨骼肌生理和病理生理中的这种双重性,并旨在从衰老导致的其他骨骼肌萎缩状况(如肌肉减少症)中获得关键见解。