Oxidative stress and damage are associated with a number of ageing phenotypes, including age-related loss of muscle mass and reduced contractile function (sarcopenia). Our group and others have reported loss of neuromuscular junction (NMJ) integrity and increased denervation as initiating factors in sarcopenia, leading to mitochondrial dysfunction, generation of reactive oxygen species and peroxides, and loss of muscle mass and weakness. Previous studies from our laboratory show that denervation-induced skeletal muscle mitochondrial peroxide generation is highly correlated to muscle atrophy. Here, we directly test the impact of scavenging muscle mitochondrial hydrogen peroxide on the structure and function of the NMJ and muscle mass and function in a mouse model of denervation-induced muscle atrophy CuZnSOD (Sod1^−/− mice, Sod1KO).

中文翻译：

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肌肉线粒体过氧化氢酶表达可防止加速肌肉减少症小鼠模型中的神经肌肉接头中断、萎缩和虚弱

氧化应激和损伤与许多衰老表型有关，包括与年龄相关的肌肉质量损失和收缩功能降低（肌肉减少症）。我们的小组和其他人报告了神经肌肉接头 (NMJ) 完整性的丧失和去神经支配增加作为肌肉减少症的起始因素，导致线粒体功能障碍、活性氧和过氧化物的产生，以及肌肉质量和虚弱的丧失。我们实验室以前的研究表明，去神经诱导的骨骼肌线粒体过氧化物的产生与肌肉萎缩高度相关。在这里，我们在去神经诱导的肌肉萎缩 CuZnSOD ( Sod1^-/-小鼠，Sod1 KO）。