脓毒症中细胞焦亡的分子机制及研究进展

Molecular mechanism of pyroptosis in sepsis

脓毒症是全世界范围内致死率很高的一种疾病,严重威胁着人类的生命健康,由于其发病机制的复杂性使得诊断治疗往往十分困难。细胞焦亡是一种新发现的伴随炎症的细胞程序性死亡方式,主要存在于许多专职吞噬的细胞中。在脓毒症中,焦亡是抵抗细菌感染所必需的,但过强的焦亡也会加重脓毒症的炎症反应。所以,对于脓毒症中细胞焦亡的信号通路及调控机制的研究可能会有助于找到潜在的治疗靶点。因此,本文总结了近年来脓毒症中细胞焦亡分子机制的一些研究进展,重点关注了参与焦亡的2条信号通路、一些有新作用的半胱氨酸天冬氨酸蛋白酶、焦亡中的关键执行者GSDM家族、脓毒症中焦亡与其他细胞死亡方式的关联。

Sepsis is a disease with a high mortality rate worldwide,which seriously threatens human life and health.Due to the complexity of its pathogenesis,diagnosis and treatment are often very difficult.Pyroptosis is a newly discovered pro-inflammatory form of progi-ammed cell death,which occurs predominantly in professional phagocytes.During sepsis,appropriate pyroptosis is required for defense against bacterial infection,however,excessive pyroptosis will also aggravate the inflammatory reaction of sepsis.Therefore,the study of the signaling pathways and regulatory mechanisms of pyroptosis in sepsis may contribute to identify potential therapeutic targets.Hence,the study provide an overview of the recent advances which focus on the two signaling pathway of pyroptosis,some caspases which have found new effects,GSDM family and the crosstalk between different form of cell death.