首页|内质网应激介导巨噬细胞极化分子机制研究进展

内质网应激介导巨噬细胞极化分子机制研究进展

扫码查看
原文链接
  • 万方数据
  • 维普
内质网(ER)是维持细胞内Ca2+稳态、折叠新合成的分泌蛋白和膜蛋白以及蛋白质翻译后修饰的重要细胞器。ER腔内错误折叠与未折叠蛋白聚集，可激活内质网应激(ERS)，进而激活蛋白激酶R样内质网激酶(PERK)、需肌醇酶1α(IRE-1α)和活化转录因子6(ATF6)三个不同的下游信号通路影响细胞的存活、分化和表型转换。近年来研究表明ERS下游信号级联反应与诱导巨噬细胞向促炎性M1型极化(IFN-γ和LPS)和抗炎性M2型极化(IL-4和IL-10)的信号通路之间存在密切相互作用，但两者之间的具体分子机制错综复杂。文中总结了 ERS介导巨噬细胞极化的主要机制，重点讨论了 ERS的三个不同下游信号影响巨噬细胞极化的分子机制。
Research progress on the molecular mechanism of endoplasmic reticulum stress-mediated macrophage polarization
The endoplasmic reticulum(ER)is an essential organelle that maintains intracellular Ca2+homeostasis,folds newly synthesized secreted and membrane proteins,and facilitates post-translational protein modifications.Misfolding and aggregation of unfolded proteins within the ER lumen can activate endoplasmic reticulum stress(ERS),which in turn activates three different downstream signaling pathways:protein kinase R-like endoplasmic reticulum kinase(PERK),inositol-requiring enzyme 1α(IRE11α),and activating transcription factor6(ATF6).These pathways affect cell survival,differentiation,and phenotype transition.Recent studies have shown a close interaction between the downstream signaling cascade of ERS and the signaling pathways that induce macrophage polarization towards pro-inflammatory M1 type(IFN-γ and LPS)and anti-inflammatory M2 type(IL-4 and IL-10).However,the specific molecular mechanisms underlying these interactions are complex and intriate.The article summarizes the primary mechanisms by which ERS mediates macrophage polarization,focusing on discussing the molecular mechanisms by which three different downstream signals of ERS affect macrophage polarization.

endoplasmic reticulum stress(ERS)macrophage polarizationprotein kinase R-like endoplasmic reticulum kinase(PERK)inositol-requiring enzyme 1α(IRE-1α)activating transcription factor 6(ATF6)review

陈伟灿、何荷番

展开 >

福建医科大学附属第二医院麻醉科,福建泉州 362000

内质网应激 巨噬细胞极化 蛋白激酶R样内质网激酶(PERK) 需肌醇酶1α(IRE-1α) 活化转录因子6(ATF6) 综述

泉州市科技局高层次人才项目

2017Z014

2024

10.13423/j.cnki.cjcmi.009808

细胞与分子免疫学杂志
中国免疫学会,第四军医大学

细胞与分子免疫学杂志

CSTPCD北大核心
影响因子：0.817
ISSN：1007-8738
年,卷(期)：2024.40(8)