文献类型：期刊文献

中文题名：ceRNA调控机制与TLR4/NF-κB通路在RA炎症中的研究进展

英文题名：Research progress on regulatory mechanisms of ceRNA and TLR4/NF-κB pathway in RA inflammation

作者：井维尧[1];杜小正[1];张星华[2];张枫帆[2];方晓丽[1];王海东[2];田杰祥[3];王若州[1];杨尚伟[1]

第一作者：井维尧

机构：[1]甘肃中医药大学针灸推拿学院,兰州730000;[2]甘肃省中医院风湿骨病科,兰州730050;[3]甘肃中医药大学附属医院风湿骨病科,兰州730000

第一机构：甘肃中医药大学针灸推拿学院

年份：2022

卷号：42

期号：4

起止页码：359

中文期刊名：现代免疫学

外文期刊名：Current Immunology

收录：CSTPCD;;北大核心:【北大核心2020】；

基金：国家自然科学基金(81960832);国家中医药管理局甘肃郑氏针法学术流派传承工作室项目(2305135901);兰州市科学技术局课题(2016-RC-50)。

语种：中文

中文关键词：类风湿关节炎;Toll样受体4/核因子κB信号通路;竞争内源性RNA;微小RNA;长链非编码RNA

外文关键词：rheumatoid arthritis;Toll-like receptor 4/nuclear factorκB signaling pathway;competing endogenous RNA;micro ribonucleic acid;long non-coding ribonucleic acid

摘要：miRNA与长链非编码RNA(long non-coding RNA,lncRNA)都属于非编码RNA,其表达水平与众多疾病的发生与发展相关。竞争内源性RNA(competing endogenous RNA,ceRNA)调控机制是lncRNA竞争性地结合miRNA并调控相关基因表达的过程。众多研究提示,ceRNA调控机制参与了类风湿关节炎(rheumatoid arthritis,RA)的发生与发展过程。同时,TLR4/NF-κB信号通路在RA中异常表达,可调控RA炎症反应,是RA炎症级联反应的核心之一。该文总结并探讨miRNA、lncRNA与RA的关系并围绕ceRNA调控机制在RA疾病中的作用。基于TLR4/NF-κB信号通路,探讨ceRNA调控机制在RA炎症中的研究进展,可为RA临床寻找新的治疗靶点提供参考。
Both miRNA and long non-coding RNA(lncRNA)belong to non-coding RNA and their expression levels correlate with the occurrence and development of many diseases.The regulatory mechanism of competing endogenous RNA(ceRNA)is a process in which lncRNA competitively binds miRNA and regulates the expression of related genes.Many studies suggestthat ceRNA regulatory mechanism is involved in the occurrence and development of rheumatoid arthritis(RA).On the other hand,TLR4/NF-κB signaling pathway which regulates inflammatory responses operates abnormally in RA and is one of the key modules in the RA inflammatory cascade.This review summarizes and discusses the relationships between miRNA,lncRNA and RA and revolves around the regulatory roles of ceRNA in RA.The article also discusses the current progress of ceRNA research in RA inflammation based on TLR4/NF-κB signaling pathway,which may provide insights into new therapeutic targets for RA.