文献类型：期刊文献

中文题名：PI3K/Akt信号通路调控哮喘气道黏液高分泌的研究现状

英文题名：Research status of PI3K/Akt signal pathway regulating airway mucus hypersecretion in asthma

作者：席建宏[1];黄柯婷[1];王志旺[1];杜玥[1];李济阳[1];庞亚蓉[1];梁可克[1]

第一作者：席建宏

机构：[1]甘肃中医药大学药学院,甘肃兰州730000

第一机构：甘肃中医药大学药学院（西北中藏药协同创新中心办公室）

年份：2022

卷号：38

期号：22

起止页码：2779

中文期刊名：中国临床药理学杂志

外文期刊名：The Chinese Journal of Clinical Pharmacology

收录：CSTPCD;;北大核心:【北大核心2020】；CSCD:【CSCD2021_2022】；

基金：国家自然科学基金资助项目(81460668);甘肃省自然科学基金资助项目(20JR5RA183,1606RJZA011,1310RJZA086)。

语种：中文

中文关键词：哮喘;磷酯酰激醇3-激酶/丝氨酸苏氨酸蛋白激酶信号通路;黏液高分泌;调控机制

外文关键词：asthma;phosphatidylethanol 3-kinase/serine threonine protein kinase signal pathway;airway mucus hypersecretion;regulation mechanism

摘要：哮喘是气道炎症性疾病,气道黏膜炎症微环境促使杯状细胞化生而引起黏液高分泌,富含炎症介质的黏液滞留在气道进一步加重气道炎症、诱发高反应性并促使气道重塑;重症哮喘黏液栓阻塞气道引起窒息、甚至猝死。磷酯酰激醇3-激酶(PI3K)/丝氨酸苏氨酸蛋白激酶(Akt)信号通路与下游靶点或细胞相互作用而参与哮喘气道黏液高分泌。本文在阐述PI3K/Akt信号通路与哮喘气道黏液高分泌的基础上,重点综述PI3K/Akt信号通路通过调控炎症细胞、核因子-κB(NF-κB)、Toll样受体(TLRs)以及丝裂原活化蛋白激酶(MAPKs)而参与哮喘气道黏液高分泌的研究现状,为哮喘气道黏液高分泌的实验研究与新药开发提供理论依据。
Asthma is an airway inflammatory disease;airway mucosal inflammatory microenvironment promotes goblet cell biochemistry and leads to high secretion of mucus,and mucus rich in inflammatory mediators remains in the airway to further aggravate airway inflammation,induces hyperresponsiveness and promotes airway remodeling;severe asthma mucus emboli blocks the airway,even resulting in asphyxia and even sudden death.Phosphatidylethanol 3-kinase(PI3K)/serine threonine protein kinase(Akt)signal pathway interacts with downstream targets or cells to participate in airway mucus hypersecretion in asthma.On the basis of expounding the relationship between PI3K/Akt signal pathway and airway mucus hypersecretion in asthma,this paper focuses on the research status of PI3K/Akt signal pathway involved in airway mucus hypersecretion in asthma by regulating inflammatory cells,nuclear factor-kappa B(NF-κB),Toll-like receptor(TLRs)and mitogen-activated protein kinase(MAPKs),so as to provide theoretical basis for experimental research and new drug development of asthma airway mucus hypersecretion.