炎性受体NOD2及NF-κB在痛风性关节炎中的研究进展  

Progress of the Inflammatory Receptor NOD2 and NF-κB in Gouty Arthritis

作　　者：陈凤 苏娟[1] 

机构地区：[1]青海大学附属医院风湿免疫科,青海 西宁

出　　处：《临床医学进展》2023年第7期11324-11328,共5页Advances in Clinical Medicine

摘　　要：痛风是最常见的晶体诱导的自身炎症性关节疾病,当高尿酸血症、血清尿酸盐持续升高导致自身组织中的尿酸盐水平过饱和,导致单钠尿酸盐(monosodium urate, MSU)晶体在关节内和关节周围形成和沉积时就会发生痛风。研究发现,MSU通过激活炎性受体NOD2通路,进而激活NF-κB炎症因子,参与痛风性关节炎的发作。本文就炎性受体NOD2及NF-κB参与痛风性关节炎的过程研究进展综述如下。Gout is the most common crystal-induced autoinflammatory joint disease, which occurs when hyperuricemia and sustained elevation of serum urate lead to oversaturation of urate levels in the own tissues, leading to the formation and deposition of monosodium urate, monosodium urate (MSU) crystals in and around the joints. We found that MSU is involved in the onset of gouty arthritis by activating the inflammatory receptor NOD2 pathway and then activating NF-κB inflammatory fac-tors. This review summarizes the involvement of the inflammatory receptor NOD2 and NF-κB in gouty arthritis.

关 键 词：炎性受体NOD2 NF-ΚB 痛风性关节炎 

分 类 号：R58[医药卫生—内分泌]