Pyroptosis, a form of programmed cell death with a high pro-inflammatory effect, causes cell lysis and leads to the secretion of countless interleukin-1β (IL-1β) and IL-18 cytokines, resulting in a subsequent extreme inflammatory response through the caspase-1-dependent pathway or caspase-1-independent pathway. Adult-onset Still’s disease (AOSD) is a systemic inflammatory disease with extensive disease manifestations and severe complications such as macrophage activation syndrome, which is characterized by high-grade inflammation and cytokine storms regulated by IL-1β and IL-18. To date, the pathogenesis of AOSD is unclear, and the available therapy is unsatisfactory. As such, AOSD is still a challenging disease. In addition, the high inflammatory states and the increased expression of multiple pyroptosis markers in AOSD indicate that pyroptosis plays an important role in the pathogenesis of AOSD. Accordingly, this review summarizes the molecular mechanisms of pyroptosis and describes the potential role of pyroptosis in AOSD, the therapeutic practicalities of pyroptosis target drugs in AOSD, and the therapeutic blueprint of other pyroptosis target drugs.

细胞焦亡是一种具有高度促炎作用的程序性细胞死亡形式，会导致细胞裂解并导致无数白细胞介素-1β (IL-1β) 和 IL-18 细胞因子的分泌，从而通过 caspase 导致随后的极端炎症反应-1依赖性途径或caspase-1非依赖性途径。成人斯蒂尔病（AOSD）是一种全身性炎症性疾病，具有广泛的疾病表现和巨噬细胞活化综合征等严重并发症，其特点是由IL-1β和IL-18调节的高度炎症和细胞因子风暴。迄今为止，AOSD的发病机制尚不清楚，可用的治疗方法也不尽如人意。因此，AOSD 仍然是一种具有挑战性的疾病。此外，AOSD中的高炎症状态和多种细胞焦亡标志物的表达增加表明细胞焦亡在AOSD的发病机制中发挥着重要作用。因此，本文总结了焦亡的分子机制，描述了焦亡在AOSD中的潜在作用、焦亡靶药物在AOSD中的治疗实用性以及其他焦亡靶药物的治疗蓝图。