PI3K/Akt/mTOR通路在脑缺血再灌注损伤的分子机制及治疗干预研究进展  

Research progress on molecular mechanism and therapeutic intervention of PI3K/Akt/mTOR pathway in cerebral ischemia-reperfusion injury

作　　者：曹靖兰(综述) 陈婷(审校) 张霞 刘金彦[2] 岳红梅[3] CAO Jinglan;CHEN Ting;ZHANG Xia;LIU Jinyan;YUE Hongmei(School of Clinical Medicine,Jining Medical University,Jining,Shandong 272067,China;Department of Nephrology,Jining First People′s Hospital,Jining,Shandong 272011,China;Department of Neurology,Jining First People′s Hospital,Jining,Shandong 272011,China)

机构地区：[1]济宁医学院临床医学院,山东济宁272067 [2]济宁市第一人民医院肾内科,山东济宁272011 [3]济宁市第一人民医院神经内科,山东济宁272011

出　　处：《现代医药卫生》2023年第16期2812-2816,共5页Journal of Modern Medicine & Health

摘　　要：及时恢复脑组织血液灌注是提高脑缺血患者生存率的最佳方式,但血流灌注恢复会导致脑组织缺血再灌注损伤。自噬是神经细胞的自我保护机制,胞内磷脂酰肌醇激酶(PI3K)/苏氨酸蛋白激酶C(Akt)/雷帕霉素靶蛋白(mTOR)通路调节细胞自噬在清除衰老损伤的细胞器、改善细胞能量代谢和减少细胞凋亡方面具有重要作用。该文主要对PI3K/Akt/mTOR信号通路介导的细胞自噬的病理、生理机制及当下的治疗干预进行综述,为改善脑缺血患者的预后及药物研发提供参考。The timely recovery of cerebral blood perfusion is the best way to improve the survival rate of patients with cerebral ischemia,however,the recovery of cerebral blood perfusion may also induce cerebral ischemia-reperfusion injury.Autophagy is the self-protection mechanism of neurons.The regulation of cell autophagy by intracellular phosphatidylinositol kinase(PI3K)/threonine protein kinase C(Akt)/target of rapamycin(mTOR)pathway plays an important role in eliminating aging damaged organelles,improving cell energy metabolism and reducing cell apoptosis.The pathophysiological mechanism of cell autophagy mediated by PI3K/Akt/mTOR signaling pathway and the current therapeutic intervention were reviewed in this article,so as to provide reference for improving the prognosis of patients with cerebral ischemia and drug research and development.

关 键 词：PI3K Akt MTOR 信号通路 脑缺血再灌注 分子机制 治疗干预 

分 类 号：R74[医药卫生—神经病学与精神病学] R54[医药卫生—临床医学]