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
杨玉娇 1吕树泉2
作者信息
- 1. 050091 石家庄,河北中医药大学研究生学院
- 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
- 折叠
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.
Abstract
Nuclear factor κB(NF-κB),the activation of signaling pathways is closely related to the development of chronic inflammation.Multiple pro-inflammatory factors activate NF-κB kinase inhibitor ε/TANK binding kinase 1(IKKε/TBK1),pancreatic islets β cellular 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 response ε/research progress on the mechanism of action IKKε/TBK1 pathway 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Key words
Diabetes mellitus,type 2/IKKε/TBK1/Signal pathway/Action mechanism引用本文复制引用
出版年
2025
NETL
NSTL
万方数据