自噬与NLRP3炎症小体激活间的相互作用

Interaction Between Autophagy and Activation of Inflammatory Bodies in NLRP3

自噬作为真核生物细胞遭遇各种应激压力时发生的一种基本应答方式,参与细胞的多种生命活动,使细胞在各种应激条件下维持一种动态平衡状态。NOD样受体家族核苷酸结合寡聚化结构域样受体3(NOD-like receptor family,pyrin domain containing 3,NLRP3)炎症小体,是生物体内防御病原微生物的固有免疫防御系统的重要组成部分。NLRP3炎症小体通过激活胱天蛋白酶-1(caspase-1),从而促进白细胞介素-1β(interleukin-1,IL-1β)和白细胞介素-18(interleukin-18,IL-18)等促炎细胞因子的成熟和分泌,继而介导炎症的发生。众多研究表明,自噬能够负向或正向调控NLRP3炎症小体的激活。同时,NLRP3炎症小体也会逆向影响自噬的作用。本文对自噬包括选择性自噬与NLRP3炎症小体激活的相互作用,以及通过激活自噬抑制NLRP3炎症小体,从而在炎症相关疾病治疗中的应用进行综述。

Autophagy,as a basic response of eukaryotes under various kinds of stress,is involved in various cellular activities,allowing cells to maintain a dynamic balance under various stress conditions.NOD-like receptor family,pyrin domain containing 3(NLRP3)inflammatory bodies are an important part of the innate immune defense system against pathogenic microorganisms.They promote the maturation and secretion of inflammatory cytokines such as interleukin-1(IL-1β)and interleukin-18(IL-18)by activating caspase-1,thus inducing inflammation.At present,numerous studies have shown that autophagy can negatively or positively regulate the activation of NLRP3 inflammasome,and NLRP3 inflammasomes can also adversely affect autophagy.This review summarizes the interaction between autophagy/mitophagy and activation of NLRP3 inflammasome,as well as its application in the treatment of inflammation-related diseases.