摘要
最初认为纤溶酶原激活（PA）系统通过两种丝氨酸蛋白酶（组织型纤溶酶原激活物（tPA）和尿激酶型纤溶酶原激活物（uPA））催化纤溶酶原转化为纤溶酶而专门促进纤维蛋白的降解。然而，过去30年积累的实验证据表明，tPA和uPA也存在于中枢神经系统（CNS）中，它们具有过多的功能，并不总是需要纤溶酶产生或纤维蛋白降解。例如，tPA和uPA的纤溶酶原依赖性和非依赖性作用在作为世界上死亡和残疾的主要原因之一的病理生理学事件中发挥核心作用：脑缺血。实际上，最近的研究表明，脑缺血发作后tPA从突触前区室快速释放可保护突触免受缺血性损伤的有害影响，uPA的分泌及其与受体的结合（uPAR）在恢复期间阶段促进已经失去急性缺血性损伤的突触的修复。 uPA的这种恢复作用具有很高的转化意义，因为到目前为止还没有有效的方法来诱导缺血性脑中的神经修复。在这里，我们将讨论最近的证据，弥合PA系统领域的基础研究与缺血性卒中患者床边之间的差距，表明uPA和uPAR是制定促进缺血性卒中幸存者神经功能恢复的治疗策略的潜在目标。 。
关键词: 组织型纤溶酶原激活物，尿激酶型纤溶酶原激活物，纤溶酶，神经修复，脑缺血，神经保护。
图形摘要
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