后肢失负荷诱导的骨骼肌萎缩中线粒体功能紊乱

Mitochondrial Dysfunction of Skeletal Muscular Atrophy Induced with Hindlimb Unloaded.

后肢失负荷模型被用于模拟空间飞行中由失重引起的骨骼肌萎缩。后肢失负荷引起线粒体结构与功能紊乱,包括线粒体的数目减少,结构受损,分布失常,生成降低,动态变化及降解受到抑制,呼吸功能及酶活性下降。线粒体结构与功能紊乱可以引发细胞内多种途径的损伤,其中包括氧化应激和细胞凋亡。应用靶向于线粒体的营养素,通过降低肌肉中的氧化损伤,促进线粒体生成,改善线粒体功能等不同作用途径,可以抑制或改善肌萎缩的发生。本文总结了后肢失负荷诱导的骨骼肌萎缩的线粒体相关机制及其防治策略。

Hindlimb unloaded model was used to mimic the effect of skeletal muscle atrophy induced by weightlessness in space flight. Hindlimb unloaded led to mitochondrial dysfunction, including mitochondrial loss, structural damage, disruption of distribution, decrease of biogenesis, repression of dynamic activity and degradation, and alterations of respiration and enzyme activity. Mitochondrial structural damage and dysfunc tion triggered various intracellular damages, including oxidative stress and apoptosis. Nutrients targeting mito chondria were used to ameliorate the muscle atrophy through the inhibition of oxidative stress, promotion mito chondrial biogenesis, and improvement mitochondrial function. This review summarized mitochondria-related mechanisms in hindlimb unloading-induced skeletal muscle atrophy and the preventive and the therapeutic ap proaches.