Overexpression of thioredoxin‐2 attenuates age‐related muscle loss by suppressing mitochondrial oxidative stress and apoptosis

Huibin Tang, Michael Kim, Myung Lee, Kellie Baumann, F. Olguin, Hao He, Yoyo Wang, B. Jiang, Shuhuan Fang, Jinguo Zhu, Kun Wang, Hui Xia, Yang Gao, Harrison B. Konsker, Emmanuel Fatodu, Marco Quarta, Justin Blonigan, T. Rando, J. Shrager
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引用次数: 4

Abstract

Skeletal muscle mass is regulated by intracellular anabolic and catabolic activities. Increased catabolic activity can shift the balance towards net protein breakdown and muscle atrophy. Mitochondrial oxidative stress activates catabolism and is linked to muscle loss. Reducing mitochondrial oxidative stress is thus a plausible approach to prevent muscle atrophy. We tested this concept in age‐dependent muscle atrophy by genetically overexpressing the mitochondrial antioxidant thioredoxin‐2 (TXN2).
硫氧还蛋白-2的过表达通过抑制线粒体氧化应激和细胞凋亡来减轻年龄相关的肌肉损失
骨骼肌质量受细胞内合成代谢和分解代谢活动的调节。分解代谢活性的增加可以使平衡向净蛋白质分解和肌肉萎缩转变。线粒体氧化应激激活分解代谢,并与肌肉损失有关。因此,减少线粒体氧化应激是预防肌肉萎缩的一种可行方法。我们通过基因过表达线粒体抗氧化剂硫氧还蛋白-2(TXN2),在年龄依赖性肌肉萎缩中测试了这一概念。
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