炎症体与细胞焦亡的相关性及对凝血功能的影响

Correlation of Inflammasomes with Pyroptosis and Effect on Coagulation Function

  • 摘要: 炎症体是细胞溶质先天免疫复合物,其中 NLRP3 作为膜损伤的炎症体传感器在诱导炎症反应中发挥重要作用。当机体感染时, NLRP3 会募集ASC 衔接子并组装成大型炎症复合物。细胞焦亡是一种程序性细胞死亡方式,依赖于细胞质中半胱天冬氨酸蛋白酶触发 Gasdermin D(GSDMD)蛋白的切割,活化的 GSDMD 在细胞膜上形成膜孔,最终导致细胞质膜破裂甚至更广泛的炎症反应。本文就炎症体与细胞焦亡之间的相关性以及对凝血功能的影响进行综述, 以期为炎症体异常增加导致 DIC 的临床治疗提供新思路。

     

    Abstract: Inflammasomes are cytosolic innate immune complexes, in which NLRP3 plays a very important role in inducing inflammation as an inflammasome sensor for membrane damage. When infection is perceived, they recruit ASC adapters and assemble into large inflammatory complexes. Pyroptosis is a programmed form of cell death that relies on the cleavage of the Gasdermin D (GSDMD) protein triggered by the caspasate protease in the cytoplasm, and the activated GSDMD forms membrane pores in the cell membrane, ultimately leading to the rupture of the cytoplasmic membrane and a broader inflammatory response. This article briefly summarizes the relationship between NLRP3 inflammasome and pyroptosis, and analyzes the relationship between NLRP3 and coagulation function, aiming to provide new ideas for intervening in DIC caused by the abnormal increase of inflammasomes.

     

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