Pigna Eva, Greco Emanuela, Morozzi Giulio, Grottelli Silvia, Rotini Alessio, Minelli Alba, Fulle Stefania, Adamo Sergio, Mancinelli Rosa, Bellezza Ilaria, Moresi Viviana
DAHFMO Unit of Histology and Medical Embryology, InterUniversity Institute of Myology, Sapienza University of Rome, Rome, Italy.
Department of Experimental Medicine, University of Perugia, Perugia, Italy.
Eur J Transl Myol. 2017 Mar 3;27(1):6406. doi: 10.4081/ejtm.2017.6406. eCollection 2017 Feb 24.
Denervation leads to the activation of the catabolic pathways, such as the ubiquitin-proteasome and autophagy, resulting in skeletal muscle atrophy and weakness. Furthermore, denervation induces oxidative stress in skeletal muscle, which is thought to contribute to the induction of skeletal muscle atrophy. Several muscle diseases are characterized by denervation, but the molecular pathways contributing to muscle atrophy have been only partially described. Our study delineates the kinetics of activation of oxidative stress response in skeletal muscle following denervation. Despite the denervation-dependent induction of oxidative stress in skeletal muscle, treatments with anti-oxidant drugs do not prevent the reduction of muscle mass. Our results indicate that, although oxidative stress may contribute to the activation of the response to denervation, it is not responsible by itself of oxidative damage or neurogenic muscle atrophy.
去神经支配会导致分解代谢途径的激活，如泛素-蛋白酶体和自噬，从而导致骨骼肌萎缩和无力。此外，去神经支配会在骨骼肌中诱导氧化应激，这被认为有助于骨骼肌萎缩的诱导。几种肌肉疾病的特征是去神经支配，但导致肌肉萎缩的分子途径仅得到了部分描述。我们的研究描绘了去神经支配后骨骼肌氧化应激反应激活的动力学。尽管骨骼肌中存在去神经支配依赖性的氧化应激诱导，但抗氧化药物治疗并不能阻止肌肉质量的减少。我们的结果表明，虽然氧化应激可能有助于激活对去神经支配的反应，但它本身并不导致氧化损伤或神经源性肌肉萎缩。
