刘雯, 郭文洁, 徐强, 孙洋. NLRP3炎症小体调控机制研究进展J. 药学学报, 2016,51(10): 1505-1512. doi: 10.16438/j.0513-4870.2016-0380
引用本文: 刘雯, 郭文洁, 徐强, 孙洋. NLRP3炎症小体调控机制研究进展J. 药学学报, 2016,51(10): 1505-1512. doi: 10.16438/j.0513-4870.2016-0380
LIU Wen, GUO Wen-jie, XU Qiang, SUN Yang. Advances in mechanisms for NLRP3 inflammasomes regulationJ. Acta Pharmaceutica Sinica, 2016,51(10): 1505-1512. doi: 10.16438/j.0513-4870.2016-0380
Citation: LIU Wen, GUO Wen-jie, XU Qiang, SUN Yang. Advances in mechanisms for NLRP3 inflammasomes regulationJ. Acta Pharmaceutica Sinica, 2016,51(10): 1505-1512. doi: 10.16438/j.0513-4870.2016-0380

NLRP3炎症小体调控机制研究进展

Advances in mechanisms for NLRP3 inflammasomes regulation

  • 摘要: 炎症小体活化是由多蛋白复合物组装信号介导的炎症相关的半胱氨酸天冬氨酸特异蛋白酶(caspase)活化以及白细胞介素-1(interleukin-1β,IL-1β)、白细胞介素-18(interleukin-18,IL-18)等炎症因子的成熟过程。其中NOD(nucleotide binding oligomerization domain)样受体家族3(NOD-like receptors,NLRP3)炎症小体是目前研究最透彻的炎症小体类型,它参与了人类众多疾病的发生发展。因此靶向NLRP3炎症小体已经成为相关疾病治疗药物开发的热点。本综述总结了近5年来关于NLRP3炎症小体的研究进展,包括NLRP3 priming阶段的调控、蛋白复合物组装的调控、内源性代谢物质及亚细胞器对NLRP3的活化调节及小分子抑制剂的研究。对NLRP3调控机制的深入认识将有助于新药物靶标发现和治疗药物的开发。

     

    Abstract: 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.

     

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