基础医学与临床 ›› 2015, Vol. 35 ›› Issue (12): 1695-1699.

• 短篇综述 • 上一篇    下一篇

痛风发病机制研究进展

董鹏,宋慧   

  1. 北京积水潭医院
  • 收稿日期:2015-05-11 修回日期:2015-10-16 出版日期:2015-12-05 发布日期:2015-12-04
  • 通讯作者: 宋慧 E-mail:jst_fsmy@126.com

Research progress in mechanisms of gout

  • Received:2015-05-11 Revised:2015-10-16 Online:2015-12-05 Published:2015-12-04

摘要: 痛风是一种由于单钠尿酸盐(MSU)晶体与组织微环境相互作用导致的反复发作的急性炎症反应。MSU晶体启动机体的炎性级联反应涉及多种信号通路,其中包括MSU晶体直接与细胞表面Toll样受体的结合,MSU晶体与细胞膜表面脂类分子的结合以及MSU晶体以内吞的方式进入细胞。NLRP3炎性小体的活化处于炎性反应的中心环节。

关键词: 痛风, 单钠尿酸盐, 炎症反应, 炎性小体

Abstract: Gout is a disease characterized by recurrent attacks of acute inflammation which triggered by interactions between endogenous monosodium urate (MSU) crystals and the local tissue environment. The mechanism by which MSU crystals activate pro-in?ammatory cells involves several signal pathways. It is described that MSU crystals could bind to Toll-like receptors. MSU crystals may also interact with cholesterol on plasma membranes. Moreover, MSU crystals phagocytosis play a critical role for the development of acute inflammation. Recent work has implicated the activation of NLRP3 in?ammasome is the core step of acute inflammation.

Key words: gout, monosodium urate, inflammation, in?ammasome

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