Department of Neurobiology, Physiology and Behavior University of California, Davis 95616, USA; Department of Membrane Biology, University of California, Davis 95616, USA.
Exp Neurol. 2013 Oct;248:129-35. doi: 10.1016/j.expneurol.2013.06.003. Epub 2013 Jun 12.
Loss of skeletal muscle mass is a serious consequence of multiple diseases and conditions for which there is limited treatment options. Disuse-induced muscle atrophy occurs as the result of both reduced mechanical loading and decreased neural activity. Hibernation represents a unique physiological state where skeletal muscles are protected from unloading, inactivity and nutritional deprivation. A recent study published in Experimental Neurology (Xu et al., 2013) utilized the thirteen-lined ground squirrel, a natural hibernator, to specifically examine whether peroxisome proliferator-activated receptor γ (PPARγ) coactivator 1-α (PGC-1α) and its associated upstream and downstream signaling partners were increased during hibernation. The results showed an increase in PGC-1α expression as well as increases in mitochondrial biogenesis, oxidative capacity, and antioxidant capacity in hibernating animals. It was suggested that upregulation of PCG-1α could be a viable strategy for the treatment of disuse-induced atrophy in humans. This commentary discusses the results of Xu et al. in the context of other studies that have examined muscle sparing in hibernating mammals, and compares these findings to what is known about disuse-induced atrophy in nonhibernating rodents and humans.
骨骼肌质量的丧失是多种疾病和病症的严重后果，而这些疾病和病症的治疗选择有限。废用性肌肉萎缩是由于机械负荷减少和神经活动减少而导致的。冬眠代表了一种独特的生理状态，在这种状态下，骨骼肌可以免受卸载、不活动和营养剥夺的影响。最近发表在《实验神经病学》（Xu 等人，2013 年）上的一项研究利用十三线地松鼠（一种天然冬眠动物）专门研究了过氧化物酶体增殖物激活受体 γ（PPARγ）共激活因子 1-α（PGC-1α）及其相关的上游和下游信号伙伴是否在冬眠期间增加。结果表明，PGC-1α 的表达增加，以及冬眠动物中线粒体生物发生、氧化能力和抗氧化能力的增加。研究人员认为，上调 PCG-1α 可能是治疗人类废用性萎缩的一种可行策略。本评论在检查冬眠哺乳动物肌肉保护的其他研究的背景下讨论了 Xu 等人的研究结果，并将这些发现与非冬眠啮齿动物和人类中已知的废用性萎缩进行了比较。
