Alway Stephen E, Mohamed Junaith S, Myers Matthew J
1Division of Exercise Physiology; 2Center for Cardiovascular and Respiratory Sciences, and Mitochondria, Metabolism, and Bioenergetics; and 3Centers for Neuroscience, West Virginia University School of Medicine, Morgantown, WV.
Exerc Sport Sci Rev. 2017 Apr;45(2):58-69. doi: 10.1249/JES.0000000000000101.
We present the hypothesis that an accumulation of dysfunctional mitochondria initiates a signaling cascade leading to motor neuron and muscle fiber death and culminating in sarcopenia. Interactions between neural and muscle cells that contain dysfunctional mitochondria exacerbate sarcopenia. Preventing sarcopenia will require identifying mitochondrial sources of dysfunction that are reversible.
功能失调的线粒体积累引发信号级联反应,导致运动神经元和肌纤维死亡,并最终导致肌肉减少症。含有功能失调线粒体的神经细胞与肌肉细胞之间的相互作用会加剧肌肉减少症。预防肌肉减少症需要识别可逆转的线粒体功能障碍来源。