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J. P. Hyatt, R. R. Roy, K. M. Baldwin and V. R. Edgerton, “Nerve Activity-Independent Regulation of Skeletal Muscle Atrophy: Role of MyoD and Myogenin in Satellite Cells and Myonuclei,” American Journal of Physiology: Cell Physiology, Vol. 285, No. 5, 2003, pp. C1161-C1173.

has been cited by the following article:

• TITLE: Overexpression of MyoD Attenuates Denervated Rat Skeletal Muscle Atrophy and Dysfunction

  AUTHORS: Wei-Min Xiong, Jia-Hui Huang, Lei Xie, Yuan Qiao, Xin-Min Lu, Jiang-Chen Peng, Jin-Jia Hu

  KEYWORDS: MyoD; Denervation; Rat Skeletal Muscle; Atrophy; Dysfunction

  JOURNAL NAME: Neuroscience and Medicine, Vol.3 No.4, December 31, 2012

  ABSTRACT: Nerve injury commonly contributes to irreversible functional impairment, reconstruction of the function of muscle is big challenge. In denervated skeletal muscle, therapid expression of MyoD mRNA and protein also occurs during early postdenervation, which suggested that the function of denervation-induced MyoD may be to prevent denervation-induced skeletal muscle atrophy. However, the detail mechanism is not clear. Therefore, in this study, we established a stable-transfected MyoD L6 cell line. After the operation for cutting the rats’ tibial nerve, the MyoD-L6 cells were injected in the gastrocnemius, the function of the gastronemius was monitored. It was found that injected the MyoD-L6 cells could attenuate the muscle atrophy and dysfunction. Therefore, overexpression of MyoD could serve as a new therapy strategy to cure denervation-induced dysfunction of skeletal muscle.