骨骼肌线粒体功能障碍和肌少症

Skeletal muscle mitochondrial dysfunction and sarcopenia

摘要:

线粒体脱氧核糖核酸突变、活性氧(ROS)产生过多、生物合成下降、动力学异常、自噬失调等引起的线粒体功能障碍可能是导致肌少症发生和发展的主要因素。运动可以改善线粒体功能,是目前最有效的肌少症治疗方法。减少线粒体ROS产生的维生素E/C、白藜芦醇以及靶向线粒体的抗氧化剂等,可以通过调控线粒体,改善肌肉数量及功能。改善线粒体功能可能是肌少症治疗的靶点。

Abstract:

Mitochondrial dysfunction caused by mitochondrial deoxyribonucleic acid mutation, excess reactive oxygen species (ROS) production, decreased biogenesis, dynamics dysregulation, and mitophagy disorder might be the main factor leading to the occurrence and development of sarcopenia. Nowadays, physical exercise, because of its enhancing or restoring mitochondrial function, has been well accepted as an essential regime in the prevention and treatment of the disease. ROS-targeted therapies, including vitamin E/C, resveratrol, and targeted antioxidants, can regulate mitochondria to improve muscle quantity and function. Improving mitochondrial function can be a target for sarcopenia treatment.