细胞焦亡是一种依赖天冬氨酸特异性半胱氨酸蛋白酶1(cysteinyl aspartate specific proteinase 1，caspase-1)/caspase-11的程序性细胞死亡方式。炎性小体的激活在细胞焦亡过程中扮演重要角色。当病原体入侵时，核苷酸结合寡聚化结构域样受体(nucleotide-binding oligomerization domain-like receptor，NLR)和黑色素瘤缺乏因子2(absent in melanoma 2，AIM2)等胞内模式识别受体(pattern recognition receptor，PRR)与相应配体结合，导致炎性小体多蛋白复合物组装和caspase-1/caspase-11激活，进而诱导细胞焦亡发生。深入研究炎性小体激活和细胞焦亡的相关机制，对认识炎症性疾病的发生发展非常重要。本文就炎性小体激活与细胞焦亡的研究进展进行综述。

Pyroptosis is a new form of programmed cell death depending on cysteinyl aspartate specific proteinase 1 (caspase-1). Inflammasome plays a significant role in regulating pyroptosis. Intracellular pattern recognition proteins such as nucleotide-binding oligomerization domain-like receptor (NLR) and absent in melanoma 2 (AIM2) act to their ligands and promote the assembly of inflammasome as well as the activation of caspase-1/caspase-11, then induce pyroptosis. The in-depth research on the mechanisms and correlation between pyroptosis and inflammasome contributes to the understanding of the occurrence and development of pyroptosis-related inflammatory diseases.