基于炎症反应探讨核因子κB激酶抑制剂ε/TANK结合激酶1通路在2型糖尿病作用机制的研究进展  

Research progress on the mechanism of IKKε/TBK1 pathway in the pathogenesis of type 2 diabetes mellitus based on inflammatory response

作　　者：杨玉娇 吕树泉[2] YANG Yujiao;LYU Shuquan(Graduate School of Hebei University of Chinese Medicine,Shijiazhuang 050091,China)

机构地区：[1]河北中医药大学研究生学院,石家庄050091 [2]河北中医药大学附属沧州中西医结合医院内分泌糖尿病科

出　　处：《中国糖尿病杂志》2025年第1期77-80,共4页Chinese Journal of Diabetes

基　　金：河北省自然科学基金(H2022110019);河北省中医药管理局科研计划项目(2021311);苏秀海全国名老中医药专家传承工作室(国中医药人教函[2022]75号)。

摘　　要：核因子κB(NF-κB)信号通路激活与慢性炎症产生密切相关。多种促炎因子激活NF-κB激酶抑制剂ε/TANK结合激酶1(IKKε/TBK1),胰岛β细胞功能低下或丧失,导致T2DM。抑制或阻断IKKε/TBK1可减少炎性因子产生,降低IR,提高IS,减少T2DM发生。本文综述基于炎症反应探讨IKKε/TBK1通路在T2DM作用机制的研究进展。Nuclear factorκB(NF-κB),the activation of signaling pathways is closely related to the development of chronic inflammation.Multiple pro-inflammatory factors activate NF-κB kinase inhibitorε/TANK binding kinase 1(IKKε/TBK1),pancreatic isletsβcellular dysfunction or loss leads to type 2 diabetes mellitus(T2DM).Inhibiting or blocking IKKε/TBK1 can reduce the production of inflammatory factors,lower insuin resistance,improve insulin sensitivity,and reduce the occurrence of T2DM.This article reviews the action mechanism based on inflammatory responseε/research progress on the mechanism of action IKKε/TBK1pathway in T2DM.

关 键 词：糖尿病 2型 核因子κB激酶抑制剂ε TANK结合激酶1 信号通路 作用机制 

分 类 号：R587.1[医药卫生—内分泌]