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缺血后脑损伤是一个复杂而迅速的级联反应过程，细胞程序性死亡在此过程中发挥着重要作用，PI3K/AKT信号通路是细胞关键的存活通路之一，在脑缺血及细胞程序性死亡中均起着重要作用。本文综述了近5年PI3K/AKT信号通路在脑缺血后细胞程序性死亡中的研究进展，旨在为缺血性脑卒中的科学研究提供新思路。检索相关数据库，结果显示，PI3K/AKT信号通路可调控神经细胞的存活/凋亡、自噬、神经发生以及神经细胞增殖和突触可塑性，并且可阻断细胞启动程序性死亡；可从细胞凋亡、坏死性凋亡、焦亡、自噬、铁死亡等5种程序性死亡方面改善缺血后的脑损伤。PI3K/AKT信号通路为治疗缺血性脑卒中及研究细胞程序性死亡的重要靶点。
Abstract：Brain injury after ischemia is a complex and rapid cascade reaction, where programmed cell death plays an important role. PI3 K/AKT signaling pathway is one of the important survival pathways, which is critical in cerebral ischemia and programmed cell death. The present study reviewed the research progress on PI3 K/AKT signaling pathway in programmed cell death after ischemic stroke in recent five years, aiming to provide new ideas for the scientific research on ischemic stroke. The Chinese and English databases were searched for the relevant research papers, such as CNKI,Wanfang Data, VIP,PubMed, Medline, and Embase. The results showed that the PI3 K/AKT signaling pathway could regulate the survival/apoptosis of neurons, autophagy, neurogenesis, neuronal proliferation, and synaptic plasticity, and block programmed cell death. It is suggested that this pathway could improve post-ischemic brain injury from five types of programmed death, including apoptosis, necroptosis, pyroptosis, autophagy, and ferroptosis. PI3 K/AKT signaling pathway is a key target for the treatment of ischemic stroke and the study of programmed cell death.
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基本信息:
DOI：10.13412/j.cnki.zyyl.20210806.002
中图分类号:R743.3
引用信息:
[1]陈海,王建.PI3K/AKT信号通路在缺血性脑卒中后细胞程序性死亡中的研究进展[J].中药药理与临床,2022,38(02):247-252.DOI:10.13412/j.cnki.zyyl.20210806.002.
基金信息:
国家自然科学基金面上项目(编号：81873023、81473371)
2021-08-06
2021-08-06
2021-08-06