Del Campo Andrea, Jaimovich Enrique, Tevy Maria Florencia
Centro de Estudios Moleculares de la Célula, ICBM, Facultad de Medicina, Universidad de Chile, 8389100 Santiago, Chile.
Centro de Genómica y Bioinformática, Facultad de Ciencias, Universidad Mayor, 8580000 Santiago, Chile.
Oxid Med Cell Longev. 2016;2016:9057593. doi: 10.1155/2016/9057593. Epub 2016 Aug 18.
Sarcopenia is the loss of muscle mass accompanied by a decrease in muscle strength and resistance and is the main cause of disability among the elderly. Muscle loss begins long before there is any clear physical impact in the senior adult. Despite all this, the molecular mechanisms underlying muscle aging are far from being understood. Recent studies have identified that not only mitochondrial metabolic dysfunction but also mitochondrial dynamics and mitochondrial calcium uptake could be involved in the degeneration of skeletal muscle mass. Mitochondrial homeostasis influences muscle quality which, in turn, could play a triggering role in signaling of systemic aging. Thus, it has become apparent that mitochondrial status in muscle cells could be a driver of whole body physiology and organismal aging. In the present review, we discuss the existing evidence for the mitochondria related mechanisms underlying the appearance of muscle aging and sarcopenia in flies and mice.
肌肉减少症是指肌肉质量的丧失，同时伴有肌肉力量和耐力的下降，是老年人残疾的主要原因。在老年人出现明显身体影响之前很久，肌肉就开始流失了。尽管如此，肌肉衰老背后的分子机制仍远未被理解。最近的研究发现，不仅线粒体代谢功能障碍，而且线粒体动力学和线粒体钙摄取都可能参与骨骼肌质量的退化。线粒体稳态影响肌肉质量，而肌肉质量反过来又可能在全身衰老信号传导中起触发作用。因此，很明显肌肉细胞中的线粒体状态可能是全身生理和机体衰老的驱动因素。在本综述中，我们讨论了果蝇和小鼠中肌肉衰老和肌肉减少症出现的线粒体相关机制的现有证据。
