INSERM U974/CNRS UMR 7215, 105 bd de l'Hôpital, 75634 Paris Cedex 13, F-75013 France.
Muscle Nerve. 2010 Jun;41(6):809-18. doi: 10.1002/mus.21624.
The muscles of mdx mice progressively deteriorate with age. We wanted to know whether this is associated with a decrease in regenerative capacity and/or changes in the mammalian target of rapamycin complex (mTOR) signaling pathway. Muscles of mdx mice aged 5 weeks, 5, 12, and 18-24 months were studied. Maximal force and muscle weight of the older mice were decreased as compared to younger adult mice. Activation of the mTOR signaling pathway, i.e., phosphorylation of Akt (also known as protein kinase B) and ribosomal protein S6 was also reduced in the older mice. Moreover, 14 days after cardiotoxin injury the degree of recovery of maximal force and muscle weight were less in the older mice. In contrast to younger mice, there was also activation of the mTOR pathway during regeneration in the older mice. Progressive muscle weakness and atrophy in mdx mouse muscle is associated with a decline in regenerative potential and changes in activation of the mTOR signaling pathway.
mdx 小鼠的肌肉随着年龄的增长逐渐恶化。我们想知道这是否与再生能力的下降和/或雷帕霉素靶蛋白复合物 (mTOR) 信号通路的变化有关。研究了 5 周、5 个月、12 个月和 18-24 个月大的 mdx 小鼠的肌肉。与年轻成年小鼠相比，年龄较大的小鼠的最大力和肌肉重量降低。mTOR 信号通路的激活，即 Akt（也称为蛋白激酶 B）和核糖体蛋白 S6 的磷酸化，在老年小鼠中也减少。此外，在心脏毒素损伤后 14 天，老年小鼠的最大力和肌肉重量的恢复程度较低。与年轻小鼠不同，老年小鼠在再生过程中也激活了 mTOR 通路。mdx 小鼠肌肉的进行性肌肉无力和萎缩与再生潜力的下降以及 mTOR 信号通路激活的变化有关。
