医学分子生物学杂志 ›› 2025, Vol. 22 ›› Issue (6): 617-622.doi: 10.3870/j.issn.1672-8009.2025.06.013

• 综述 • 上一篇    下一篇

RIG-Ⅰ与疾病的相关研究进展

王文亮1, 田海萍1, 刘太乙2, 王晟3   

  1. 内蒙古医科大学第一附属医院1心血管内科,3风湿免疫科 呼和浩特市,0100002内蒙古自治区中医医院 呼和浩特市,010000
  • 收稿日期:2025-03-28 出版日期:2025-11-30 发布日期:2025-12-25
  • 通讯作者: 田海萍(E-mail:20010022@immu.edu.cn),王晟(E-mail:672608016@qq.com)
  • 基金资助:
    内蒙古自治区自然科学基金(No.2023QN08002),内蒙古医科大学一般项目(No.YKD022MS005),内蒙古自治区高层次人才研究支持基金(No.186),内蒙古自治区留学回区人员创新启动支持计划(2022),内蒙古自治区人才开发基金(2023),内蒙古医科大学附属医院高层次人才培养-续航人才(2024)

Advances in Researches on RIG-I in Diseases

WANG Wenliang1, TIAN Haiping1, LIU Taiyi2, WANG Cheng3   

  1. 1Department of Cardiovascular Medicine,3Department of Rheumatology and Immunology,First Affiliated Hospital of Inner Mongolia Medical University,Hohhot,010000,China 2Inne Mongolia Automomous Region Hospital of Traditional Chinese Medicine,Hohhot,010000,China
  • Received:2025-03-28 Online:2025-11-30 Published:2025-12-25
  • Contact: TIAN Haiping(E-mail:20010022@immu.edu.cn),WANG Cheng(E-mail:672608016@qq.com)
  • Supported by:
    Inner Mongolia Autonomous Region Natural Science Foundation(No.2023QN08002),Inner Mongolia Medical University General Project(No.YKD022MS005),Inner Mongolia Autonomous Region High level Talent Research Support Fund(No.186),Inner Mongolia Autonomous Region Study Abroad Returned Personnel Innovation Launch Support Plan(2022),Inner Mongolia Autonomous Region Talent Development Fund(2023),Inner Mongolia Medical University Affiliated Hospital High level Talent Training-Continuing Talent(2024)

摘要: 视黄酸诱导基因Ⅰ(retinoic acid inducible gene protein Ⅰ,RIG-Ⅰ)作为胞质模式识别受体,能够识别RNA病毒并通过构象变化来激活线粒体抗病毒信号蛋白(mitochondrial antiviral signaling protein,MAVS),触发TBK1-IRF3/IKK-NF-κB通路诱导Ⅰ型干扰素(type Ⅰ interferons,IFN-Ⅰ)产生。RIG-Ⅰ编码基因DDX58的突变或RIG-Ⅰ的过度激活会致使IFN-Ⅰ等炎症因子过量表达,促进细胞凋亡和自身抗体形成,造成心、脑、肾等多脏器的损伤。RIG-Ⅰ近几年在感染性疾病和非感染性疾病中的“跨界”作用受到广泛关注,文章综述了RIG-Ⅰ及其在系统性红斑狼疮、肿瘤、心血管等疾病中的作用。

关键词: RIG-I, 先天免疫, 自身免疫性疾病, 肿瘤, 心血管系统疾病

Abstract: Retinoic acid-induced gene Ⅰ(RIG-Ⅰ),served as a cytoplasmic pattern recognition receptor,is capable of recognizing RNA viruses,and can activate mitochondrial antiviral signaling protein(MAVS)through conformational changes and trigger the TBK1-IRF3/IKK-NF-κB pathway to induce type I interferon(IFN-Ⅰ)production.Mutations in the RIG-I encoding gene DDX58 or excessive activation of RIG-I can lead to the overproduction of inflammatory mediators such as IFN-I,promoting apoptosis and autoantibody formation,resulting in damage to multiple organs including the heart,brain,and kidneys.The cross-disease role of RIG-I in both infectious and non-infectious diseases has gained significant attention in recent years.This article reviews RIG-Ⅰand its roles in systemic lupus erythematosus,tumors,and cardiovascular diseases.

Key words: RIG-I, innate immunity, autoimmune diseases, tumor, cardiovascular diseases

中图分类号: