炎症体
上睑下垂
促炎细胞因子
机制(生物学)
程序性细胞死亡
细胞生物学
模式识别受体
信号转导
半胱氨酸蛋白酶1
受体
胞浆
免疫学
化学
生物
细胞凋亡
炎症
先天免疫系统
酶
认识论
生物化学
哲学
作者
Li Wang,Arthur V. Hauenstein
标识
DOI:10.1016/j.mam.2020.100889
摘要
NLRP3 is the best characterized cytosolic nod-like pattern recognition receptor which can detect microbial motifs, endogenous danger and stress signals. Activation of NLRP3 leads to the formation of a cytosolic multiprotein signaling complex called the inflammasome, which serves as a platform for caspase-1 activation leading to the processing of proinflammatory cytokines IL-1β, IL-18 and GSDMD mediated cell death. This form of pyroptotic cell death represents a major pathway of inflammation. Growing evidence has indicated hyperactivation of NLRP3 inflammasome is involved in a wide range of inflammatory diseases. In this review we present the recent advances in understanding the mechanism of NLRP3 activation, its role in driving inflammatory diseases, and the development of NLRP3 targeted therapies.
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