NLRP3炎症小体在类风湿关节炎中的研究进展  

Research Progress of NLRP3 Inflammasome in Rheumatoid Arthritis

作　　者：陈佳慧 曾家顺 CHEN Jiahui;ZENG Jiashun(Guizhou Medical University,Guiyang 550004,China;Department of Rheumatology,Affiliated Hospital of Guizhou Medical University,Guiyang 550004,China)

机构地区：[1]贵州医科大学,贵阳550004 [2]贵州医科大学附属医院风湿免疫科,贵阳550004

出　　处：《医学综述》2024年第1期98-102,107,共6页Medical Recapitulate

基　　金：贵州省中医药管理局中医药、民族医药科学技术研究课题(QZYY-2021-005);贵州医科大学附属医院国家自然科学基金培育项目(gyfynsfc[2020]-44)。

摘　　要：类风湿关节炎(RA)是一种慢性自身免疫性疾病,主要表现为多关节肿胀、疼痛、僵硬和活动受限,其基本病理改变为滑膜炎症持续发作,造成软骨和骨骼损伤,最终导致关节畸形,功能丧失。核苷酸结合寡聚化结构域样受体蛋白3(NLRP3)炎症小体通过促进炎症反应及免疫调节参与RA的发病过程,而NLRP3炎症小体激活机制及其在RA中的致病机制尚不明确。近年来,有关RA领域NLRP3炎症小体的相关研究逐渐增多,RA中NLRP3炎症小体激活后的促炎机制、免疫调节机制以及通过靶向NLRP3炎症小体治疗RA是目前的研究热点。Rheumatoid arthritis(RA)is a chronic autoimmune disease characterized by swelling,pain,stiffness,and limited mobility of multiple joints.Its basic pathological changes are persistent synovitis,causing damage to cartilage and bones,ultimately leading to joint deformities and loss of function.Nucleotide-binding oligomeric domain-like receptor protein 3(NLRP3)inflammasomes participate in the pathogenesis of RA by promoting inflammatory response and immune regulation.However,the activation mechanism of NLRP3 inflammasomes and their pathogenic mechanism in RA are still unclear.In recent years,there has been a gradual increase in research on NLRP3 inflammasomes in the field of RA.The pro-inflammatory and immunomodulatory mechanisms after NLRP3 inflammasomes activation in RA,as well as the treatment of RA by targeting NLRP3 inflammasomes,are currently the research hotspots.

关 键 词：类风湿关节炎 核苷酸结合寡聚化结构域样受体蛋白3 炎症小体 致病机制 

分 类 号：R593.22[医药卫生—内科学]