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SphK1/S1P信号通路在脑缺血再灌注神经细胞损伤机制中的研究进展

李轼 吕蔓华

中国卒中杂志2018,Vol.13Issue(12):1327-1331,5.
中国卒中杂志2018,Vol.13Issue(12):1327-1331,5.DOI:10.3969/j.issn.1673-5765.2018.12.020

SphK1/S1P信号通路在脑缺血再灌注神经细胞损伤机制中的研究进展

Progress of SphK1/S1P Signaling Pathway in the Mechanism of Cerebral Ischemia Reperfusion Injury

李轼 1吕蔓华1

作者信息

  • 1. 150001 哈尔滨哈尔滨医科大学附属第一医院神经内科
  • 折叠

摘要

Abstract

Sphingomyelin and its metabolites [ceramide, sphingosine (Sph), sphingosine-1-phosphate (S1P)] being important signaling molecules play an very important role in pathophysiological processes such as cell proliferation, survival, apoptosis and immune response. Sphingosine kinase (SphK) is a key enzyme catalyzing Sph to S1P. Cerebral ischemia reperfusion injury involves various mechanism such as excitotoxicity, neuroinflammation and oxidative stress, free radical production, blood brain barrier injure, vascular permeability alteration and cell apoptosis. This article introduced the functional characteristics of SphK1 and S1P, the effect of SphK1/S1P signaling pathway on nerve cell injury in cerebral ischemia reperfusion and the possible molecular mechanism.

关键词

鞘氨醇激酶1/鞘氨醇-1-磷酸/缺血再灌注损伤/神经炎症

Key words

SphK1/ S1P/ Ischemia reperfusion injury/ Neuroinflammation

引用本文复制引用

李轼,吕蔓华..SphK1/S1P信号通路在脑缺血再灌注神经细胞损伤机制中的研究进展[J].中国卒中杂志,2018,13(12):1327-1331,5.

基金项目

国家自然科学基金青年基金项目(81801185) (81801185)

中国卒中杂志

OACSTPCD

1673-5765

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