Key Laboratory of Neuroregeneration of Jiangsu and Ministry of Education, Co-Innovation Center of Neuroregeneration, NMPA Key Laboratory for Research and Evaluation of Tissue Engineering Technology Products, Medical College, Nantong University, Nantong, Jiangsu Province 226001, China.
Department of Endocrinology, Binhai County People's Hospital, Yancheng, Jiangsu Province 224500, China.
Biochem Pharmacol. 2023 Aug;214:115664. doi: 10.1016/j.bcp.2023.115664. Epub 2023 Jun 16.
Oxidative stress, inflammation, mitochondrial dysfunction, reduced protein synthesis, and increased proteolysis are all critical factors in the process of muscle atrophy. In particular, oxidative stress is the key factor that triggers skeletal muscle atrophy. It is activated in the early stages of muscle atrophy and can be regulated by various factors. The mechanisms of oxidative stress in the development of muscle atrophy have not been completely elucidated. This review provides an overview of the sources of oxidative stress in skeletal muscle and the correlation of oxidative stress with inflammation, mitochondrial dysfunction, autophagy, protein synthesis, proteolysis, and muscle regeneration in muscle atrophy. Additionally, the role of oxidative stress in skeletal muscle atrophy caused by several pathological conditions, including denervation, unloading, chronic inflammatory diseases (diabetes mellitus, chronic kidney disease, chronic heart failure, and chronic obstructive pulmonary disease), sarcopenia, hereditary neuromuscular diseases (spinal muscular atrophy, amyotrophic lateral sclerosis, and Duchenne muscular dystrophy), and cancer cachexia, have been discussed. Finally, this review proposes the alleviation oxidative stress using antioxidants, Chinese herbal extracts, stem cell and extracellular vesicles as a promising therapeutic strategy for muscle atrophy. This review will aid in the development of novel therapeutic strategies and drugs for muscle atrophy.
氧化应激、炎症、线粒体功能障碍、蛋白质合成减少和蛋白水解增加都是肌肉萎缩过程中的关键因素。特别是，氧化应激是引发骨骼肌萎缩的关键因素。它在肌肉萎缩的早期阶段被激活，并可以被各种因素调节。氧化应激在肌肉萎缩发展中的机制尚未完全阐明。本综述概述了骨骼肌中氧化应激的来源，以及氧化应激与炎症、线粒体功能障碍、自噬、蛋白质合成、蛋白水解和肌肉再生在肌肉萎缩中的相关性。此外，还讨论了氧化应激在几种病理状况引起的骨骼肌萎缩中的作用，包括去神经、失负荷、慢性炎症性疾病（糖尿病、慢性肾病、慢性心力衰竭和慢性阻塞性肺疾病）、少肌症、遗传性神经肌肉疾病（脊髓性肌萎缩症、肌萎缩侧索硬化症和杜氏肌营养不良症）和癌症恶病质。最后，本综述提出了使用抗氧化剂、中草药提取物、干细胞和细胞外囊泡来缓解氧化应激作为肌肉萎缩的一种有前途的治疗策略。本综述将有助于开发肌肉萎缩的新型治疗策略和药物。
