腺苷酸活化蛋白激酶与血管性认知障碍  

Adenosine monophosphate-activated protein kinase and vascular cognitive impairment

作　　者：齐倩倩[1] 滕振杰[1] 谢小华 董艳红[1] 吕佩源[1] Qi Qianqian;Teng Zhenjie;Xie Xiaohua;Dong Yanhong;Lyu Peiyuan(Department of Neurology,Hebei General Hospital,Hebei Key Laboratory of Brain Network and Cognitive Disorders,Shijiazhuang 050051,China)

机构地区：[1]河北省人民医院神经内科,河北省脑网络与认知障碍疾病重点实验室,石家庄050051

出　　处：《中华行为医学与脑科学杂志》2024年第6期567-571,共5页Chinese Journal of Behavioral Medicine and Brain Science

基　　金：科技部科技创新2030-"脑科学与类脑研究"重大项目课题(2021ZD0201807);河北省自然科学基金(H2022307075);河北省高端人才支持计划(冀办[2019]63号)。

摘　　要：腺苷酸活化蛋白激酶(adenosine monophosphate-activated protein kinase,AMPK)是一种高度保守的丝氨酸/苏氨酸激酶,在调节全身细胞能量代谢的稳态中起着至关重要的作用。在缺血、缺氧等应激状态下,AMPK可以被激活,进而调节机体氧化应激、自噬、细胞凋亡、神经炎性反应等病理过程,从而发挥神经保护作用。研究发现,慢性脑灌注不足可能是引起血管性认知障碍(vascular cognitive impairment,VCI)的一个主要原因。AMPK可以通过调节上述病理过程,对VCI产生神经保护作用。因此,本文对AMPK的分子生物学特性及其在VCI中的作用及机制进行了综述,旨在促进对AMPK的进一步研究,使其成为VCI治疗的一个新靶点。Adenosine monophosphate-activated protein kinase(AMPK)is a highly conserved serine/threonine protein kinase which plays an important role in regulating energy metabolism of the systemic cells.Under stress conditions,such as ischemia and hypoxia,AMPK can be activated.Then it plays a neuroprotective role in regulating mechanisms such as oxidative stress,autophagy,apoptosis and neuroinflammation and so on.Researches have found that chronic cerebral hypoperfusion may be a major cause of vascular cognitive impairment(VCI).AMPK can exert neuroprotective effects on VCI by regulating the aforementioned pathological processes.Therefore,this article reviews the molecular biological characteristics of AMPK and its role and mechanism in VCI,with the aim of promoting further research on AMPK and making it a new target for VCI treatment.

关 键 词：腺苷酸活化蛋白激酶 血管性认知障碍 氧化应激 自噬 神经炎性反应 凋亡 

分 类 号：R749.13[医药卫生—神经病学与精神病学]