Zhao Ethan Y, Efendizade Aslan, Cai Lipeng, Ding Yuchuan
a Departmentof Neurosurgery , Wayne State University School of Medicine , Detroit , MI 48201 , USA.
b Michigan State University College of Osteopathic Medicine , East Lansing , MI 48825 , USA.
Neurol Res. 2016 Apr;38(4):301-8. doi: 10.1080/01616412.2015.1133024. Epub 2016 Apr 19.
Stroke is a leading cause of long-term disability and death in the United States. Currently, tissue plasminogen activator (tPA), is the only Food and Drug Administration-approved treatment for acute ischemic stroke. However, the use of tPA is restricted to a small subset of acute stroke patients due to its limited 3-h therapeutic time window. Given the limited therapeutic options at present and the multi-factorial progression of ischemic stroke, emphasis has been placed on the discovery and use of combination therapies aimed at various molecular targets contributing to ischemic cell death. Protein kinase C (PKC) and Akt (protein kinase B) are serine/threonine kinases that play a critical role in mediating ischemic-reperfusion injury and cellular growth and survival, respectively. The present review will examine the role of PKC and Akt in the cellular response to ischemic-reperfusion injury.
中风是美国长期残疾和死亡的主要原因。目前,组织型纤溶酶原激活剂(tPA)是美国食品药品监督管理局批准的唯一用于急性缺血性中风的治疗方法。然而,由于其3小时的治疗时间窗有限,tPA的使用仅限于一小部分急性中风患者。鉴于目前治疗选择有限以及缺血性中风的多因素进展情况,人们已将重点放在发现和使用针对导致缺血性细胞死亡的各种分子靶点的联合疗法上。蛋白激酶C(PKC)和Akt(蛋白激酶B)是丝氨酸/苏氨酸激酶,分别在介导缺血再灌注损伤以及细胞生长和存活中起关键作用。本综述将探讨PKC和Akt在细胞对缺血再灌注损伤反应中的作用。