Liu Wen, Guo Wen-jie, Xu Qiang, Sun Yang
Yao Xue Xue Bao. 2016 Oct;51(10):1505-12.
Activation of inflammasomes involves multi-protein assembly and activation of inflammatory caspase and maturation of pro-inflammatory cytokines interleukin-1β(IL-1β) and interleukin-18(IL-18). Among those types of inflammasomes, NOD (nucleotide binding oligomerization domain)-like receptors(NLRP3) is the most studied inflammasome which involves in amount of human inflammatory and autoimmune diseases. Therefore, targeting on NLRP3 inflammasome has been one of the promising methods for treatment of diseases. In this review, we focused on the studies in the latest five years on the mechanisms of NLRP3 inflammasome regulation which mainly including NLRP3 priming, three protein complex assembly and regulation of NLRP3 inflammasome activation by endogenous metabolic compounds, iron flux, subcellular structure, other types of cells and small molecular compounds. Better understanding of NLRP3 inflammasome will be benefit for potential drug target and treatment of NLRP3 inflammasome-associated diseases.
炎性小体的激活涉及多蛋白组装、炎性半胱天冬酶的激活以及促炎细胞因子白细胞介素-1β(IL-1β)和白细胞介素-18(IL-18)的成熟。在这些类型的炎性小体中,NOD(核苷酸结合寡聚化结构域)样受体(NLRP3)是研究最多的炎性小体,它涉及多种人类炎症和自身免疫性疾病。因此,靶向NLRP3炎性小体一直是治疗疾病的有前景的方法之一。在这篇综述中,我们重点关注了近五年关于NLRP3炎性小体调控机制的研究,主要包括NLRP3的启动、三种蛋白复合物的组装以及内源性代谢化合物、铁通量、亚细胞结构、其他类型细胞和小分子化合物对NLRP3炎性小体激活的调控。更好地理解NLRP3炎性小体将有助于发现潜在的药物靶点并治疗与NLRP3炎性小体相关的疾病。