Abstract

Skeletal muscle atrophy is a complex physiological process characterized by progressive muscle mass and strength loss. It is associated with various health conditions, including aging, disease, and certain diseases. Emerging research has indicated that oxidative stress plays a significant role in developing and progressing skeletal muscle atrophy. This review article explores the mechanisms by which oxidative stress influences skeletal muscle atrophy and its implications for potential therapeutic interventions. The review begins by providing an overview of skeletal muscle atrophy and the current understanding of its underlying mechanisms, highlighting the intricate balance between protein degradation and synthesis pathways. Subsequently, the concept of oxidative stress is introduced, discussing its sources and the intricate redox signaling pathways present in skeletal muscle cells. This review's main focus is exploring the multifaceted role of oxidative stress in skeletal muscle atrophy. The detrimental effects of excessive reactive oxygen species (ROS) production on cellular components, including proteins, lipids, and deoxyribonucleic acid (DNA), are discussed. In addition, the impact of oxidative stress on key signaling pathways involved in muscle wasting, such as the ubiquitin-proteasome system and autophagy, is examined. Furthermore, the review highlights the implications of oxidative stress in modulating muscle regeneration and the importance of redox balance in maintaining muscle health. Potential therapeutic strategies targeting oxidative stress, such as antioxidant supplementation, exercise interventions, and pharmacological approaches, are also discussed. In conclusion, this review comprehensively explains the intricate relationship between oxidative stress and skeletal muscle atrophy. By elucidating the underlying mechanisms and discussing potential therapeutic interventions, this review aims to contribute to the development of novel strategies for mitigating muscle wasting and improving overall muscle health.

Full Text
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