中性粒细胞胞外捕获物在痛风发病机制中的作用机制

IF 3.4 4区 医学 Q2 RHEUMATOLOGY Clinical and experimental rheumatology Pub Date : 2024-11-01 Epub Date: 2024-06-19 DOI:10.55563/clinexprheumatol/ezzfbt
Tingting Chen, Jingguo Zhou, Wantai Dang
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引用次数: 0

摘要

痛风是一种自限性炎症性疾病,由于嘌呤代谢异常,单钠尿酸盐(MSU)结晶沉积在关节和周围组织中。中性粒细胞胞外陷阱(NET)是中性粒细胞为应对病原体攻击而形成的。在痛风期间,MSU 晶体诱导的 NETs 会加剧炎症,而聚集的 NETs(aggNETs)则通过包裹 MSU 晶体、降解细胞因子和趋化因子以及阻止中性粒细胞的募集和活化,促进痛风相关炎症的消退。随着疾病的发展,NETs 参与形成牙石。因此,NETs侵蚀是痛风自发消退的一种可能机制。研究NET影响痛风患者炎症爆发和自发消退的具体机制非常重要。本综述总结了NETs在痛风不同阶段的作用以及NETs在痛风中的具体发病机制,为痛风的诊断和治疗提供新思路。
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Mechanism of neutrophil extracellular traps in the pathogenesis of gout.

Gout is a self-limited inflammatory disease caused by the deposition of monosodium urate (MSU) crystals in joints and surrounding tissues due to abnormal purine metabolism. Neutrophil extracellular traps (NETs) are formed by neutrophils in response to pathogen attack. During gout, NETs induced by MSU crystals exacerbate inflammation, and aggregated NETs (aggNETs) promote the resolution of gout-associated inflammation by encapsulating MSU crystals, degrading cytokines and chemokines, and blocking the recruitment and activation of neutrophils. With disease progression, NETs participate in the formation of tophi. Therefore, aggNETs are a possible mechanism of spontaneous gout regression. Studying the specific mechanism by which NETs affect inflammatory bursts and spontaneous regression in gout patients is important. This review summarises the role of NETs in different stages of gout and the specific pathogenesis of NETs in gout to provide new ideas for the diagnosis and treatment of gout.

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来源期刊
CiteScore
6.10
自引率
18.90%
发文量
377
审稿时长
3-6 weeks
期刊介绍: Clinical and Experimental Rheumatology is a bi-monthly international peer-reviewed journal which has been covering all clinical, experimental and translational aspects of musculoskeletal, arthritic and connective tissue diseases since 1983.
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