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肿瘤坏死因子-α介导的信号网络调控哮喘气道黏液高分泌的研究现状     被引量:10

New research progress of tumor necrosis factor-αsignaling pathway regulating airway mucus hypersecretion in asthma

文献类型:期刊文献

中文题名:肿瘤坏死因子-α介导的信号网络调控哮喘气道黏液高分泌的研究现状

英文题名:New research progress of tumor necrosis factor-αsignaling pathway regulating airway mucus hypersecretion in asthma

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

第一作者:黄柯婷

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:2023

卷号:39

期号:9

起止页码:1344

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:【CSCD2023_2024】;

基金:国家自然科学基金资助项目(82260852;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:支气管哮喘;黏液高分泌;肿瘤坏死因子-α;杯状细胞;黏蛋白5ac

外文关键词:bronchial asthma;mucus hypersecretion;tumor necrosis factor-α;goblet cells;mucin 5ac

摘要:哮喘是气道慢性炎症性疾病,炎症反应进一步引起气道黏液高分泌,而大量黏液滞留在气道影响了肺功能,甚至阻塞小气道而引起猝死。辅助型T细胞2(Th2)细胞优势应答是哮喘的免疫学基础,肿瘤坏死因子-α(TNF-α)作为Th2细胞的主要细胞因子,在哮喘气道上皮杯状细胞(GC)增生、黏蛋白5ac(Muc5ac)过表达以及黏液高分泌过程中发挥了关键的调控作用,故TNF-α介导哮喘黏液高分泌的信号网络已成为近年来研究的热点。本文从转化生长因子β1(TGF-β1)、Toll样受体4(TLR4)、核因子-κB(NF-κB)、信号转导和转录激活因子6(STAT6)及丝裂原活化蛋白激酶(MAPK)等信号网络的角度,综述TNF-α调控哮喘气道黏液高分泌的作用机制,为哮喘气道黏液高分泌的基础研究与新药开发提供理论依据。
Asthma is a chronic inflammatory disease of the airway.The inflammatory response further causes the hypersecretion of airway mucus,and a large amount of mucus is retained in the airway,which affects lung function and even causes sudden death by blocking small airways.Helper tlymphocyt 2(Th2)cell dominant response is the immunological basis of asthma.Tumor necrosis factor-α(TNF-α),as the main cytokine of Th2 cells,plays a key regulatory role in the proliferation of airway epithelial goblet cells(GC),overexpression of mucin 5ac(Muc5ac)and mucus hypersecretion in asthma.Therefore,the signal network of TNF-α-mediated mucus hypersecretion in asthma has become a research hotspot in recent years.This article reviews the mechanism of TNF-αregulating airway mucus hypersecretion in asthma from the perspective of transforming growth factorβ1(TGF-β1),Toll-like receptors4(TLR4),nuclear factor kappa-B(NF-kB),signal transducers and activators of transcription(STAT6)and mitogen-activated protein kinase(MAPK)signaling networks,and provides a theoretical basis for basic research and new drug development of airway mucus hypersecretion in asthma.

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