中国神经再生研究(英文版) ›› 2018, Vol. 13 ›› Issue (2): 232-233.doi: 10.4103/1673-5374.226384

• 观点:脑损伤修复保护与再生 • 上一篇    下一篇

尿激酶型纤溶酶原激活剂促进缺血性脑组织中的突触修复

  

  • 收稿日期:2018-02-03 出版日期:2018-02-15 发布日期:2018-02-15

Urokinase-type plasminogen activator promotes synaptic repair in the ischemic brain

Ariel Diaz1, 2, Manuel Yepes1, 2, 3   

  1. 1 Department of Neurology and Center for Neurodegenerative Disease, Emory University School of Medicine, Atlanta, GA, USA;
    2 Division of Neuropharmacology and Neurologic Diseases, Yerkes National Primate Research Center, Atlanta, GA, USA;
    3 Department of Neurology, Veterans Affairs Medical Center, Atlanta, GA, USA
  • Received:2018-02-03 Online:2018-02-15 Published:2018-02-15
  • Contact: Manuel Yepes, M.D., myepes@emory.edu.
  • Supported by:

    This work has been supported in part by National Institutes of Health Grants NS-091201 (to MY) and NS-079331 (to MY), and VA MERIT Award IO1BX003441 (to MY).

摘要:

orcid: 0000-0002-5224-9663 (Manuel Yepes)

Abstract:

The central nervous system has a very high energy requirement. Accordingly,despite representing only 2% of the body’s mass, the brain uses 20% of the total oxygen consumption. Importantly, because most of this energy is used to maintain synaptic activity, even a mild decrease in its supply to the brain has deleterious implications for synaptic function.For example, only one minute of interruption of the cerebral blood flow during an acute ischemic stroke (AIS) is enough to destroy approximately 14 billion synapses (Saver, 2006). Importantly, because synaptic dysfunction leads to functional impairment, cerebral ischemia is one of the leading cause of disability in the world. Unfortunately, to this date there is no effective therapeutic strategy to promote neurological recovery among AIS survivors. Here we will discuss recent data indicating that binding of the serine proteinase urokinase-type plasminogen activator (uPA) to its receptor (uPAR) promotes synaptic repair in the ischemic brain, and will argue that this discovery has significant translational implications for the treatment of the rapidly growing number of patients that survive an AIS.