摘要
骨骼肌萎缩发生于多种生理和疾病状态下,如废用、衰老和慢性病。核因子-κB(NFκB)信号通路包括NF-κB、抑制蛋白-κB(IκB)和IκB激酶(IKK),它们在肌萎缩中起着重要作用,能够引起肌肉蛋白质降解、诱导炎症、阻断损伤/萎缩后肌纤维的再生。NF-κB转录靶包括MuRF-1、YY1和MMP-9,还可通过转录后机制调节MyoD。而且,应用遗传操作小鼠模型已证明NF-κB还是防止骨骼肌萎缩的重要分子靶标。该文将综述NF-κB在骨骼肌萎缩中的作用,为开发新的方法治疗肌萎缩提供参考。
Skeletal muscle atrophy occurs as a serious sydrome of a wide range of diseases and physiological conditions such as disuse, aging and various chronic diseases. Nuclear factor-kappa B （NF-κB） signaling pathway consists ofNF-κB, Ird3 and IKK. Emerging evidence suggests that activation of NF-κB in skeletal muscle may contribute to the degradation of specific muscle proteins, induce inflammation, and block the regeneration of myofibers after injury/atrophy, eventually leading to muscle atrophy. Transcriptional targets of NF-κB transpcription factor include MuRF1, YY1, MMP-9, etc. Moreover, NF-κB signaling may relulate the expression level of MyoD by post-transcriptional mechanisms. Recent studies using genetic mouse models have provided strong evidence that NF-κB could serve as an important molecular target for the prevention of skeletal muscle loss. In this review, the current understanding regarding the role of NF-κB in different models of muscle atrophy and the development of novel therapy will be discussed.
出处
《中国细胞生物学学报》
CAS
CSCD
2011年第8期942-947,共6页
Chinese Journal of Cell Biology
基金
湖北省自然科学基金(No.2010CD060)资助项目~~
