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The Double-Edged Sword of ROS in Muscle Wasting and COPD: Insights from Aging-Related Sarcopenia.

Stanley M H ChanStavros SelemidisRoss Vlahos
Published in: Antioxidants (Basel, Switzerland) (2024)
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.
Keyphrases
  • skeletal muscle
  • reactive oxygen species
  • chronic obstructive pulmonary disease
  • cell death
  • dna damage
  • insulin resistance
  • lung function
  • type diabetes
  • metabolic syndrome
  • air pollution
  • high intensity