中国神经再生研究(英文版) ›› 2020, Vol. 15 ›› Issue (5): 859-860.doi: 10.4103/1673-5374.268899

• 观点:神经损伤修复保护与再生 • 上一篇    下一篇

糖原合成酶激酶3:轴突再生的关键调节剂

  

  • 出版日期:2020-05-15 发布日期:2020-05-30

Glycogen synthase kinase 3: a crucial regulator of axotomy-induced axon regeneration

Jinlian Liu1, Qing Zhou1, Chaoqun Liu1, Chunfeng Liu1, Saijilafu2,3   

  1. 1Department of Orthopedic Surgery, Suzhou Kowloon Hospital, Shanghai Jiaotong University Medical School, Suzhou, Jiangsu
    Province, China 
    2Orthopedic Institute, Medical College, Soochow University, Suzhou, Jiangsu Province, China  3Department of Orthopedic Surgery, the First Affiliated Hospital, Soochow University, Suzhou, Jiangsu Province, China
  • Online:2020-05-15 Published:2020-05-30
  • Contact: Saijilafu, MD, PhD, saijilafu@suda.edu.cn.
  • Supported by:
    Dr. Saijilafu was supported by the National Natural Science Foundation of China (Nos. 81772353 and 81571189), the National Key Research and Development Program (No. 2016YFC 1100203), the Priority Academic Program Development of Jiangsu Higher Education Institutions, and Innovation and Entrepreneurship Program of Jiangsu Province of China.

摘要: orcid: 0000-0003-2290-9808 (Saijilafu)

Abstract: Following nerve injury, axonal disconnection in neurons usually results in persistent functional deficits, such as paralysis. However, axons in the adult mammalian central nervous system (CNS) have very limited regenerative ability. Understanding the molecular mechanism of controlling axon regeneration can provide idea for the design of effective therapeutic interventions for CNS injury, such as spinal cord injuries. Efficient axonal regeneration is achieved via gene expression in the neuronal soma, axonal transport of raw materials along the shaft, and membrane and cytoskeleton assembly at the nerve growth cone. Each process is delicately regulated by spatial-temporal controlled signaling pathways that target distinct effectors. Gene expression in the neuronal soma, especially of transcription factors, is often activated immediately following nerve injury.