脓毒症时细胞焦亡的分子机制及研究进展

Advances in the Molecular Mechanisms on Pyroptosis in Sepsis

脓毒症是宿主对感染的反应失调而导致的危及生命的器官功能障碍。脓毒症与脓毒性休克是重症患者死亡的主要原因之一。细胞焦亡是一种特定的细胞程序性死亡方式,其特征为炎症因子释放和细胞肿胀破裂。适度的细胞焦亡可以防御病原微生物感染,减轻脓毒症时组织损伤,过度的细胞焦亡可能加重脓毒症或造成继发感染。经典和非经典炎性体在细胞焦亡中发挥关键作用,消皮素D、泛连接蛋白-1对诱导并调控细胞焦亡至关重要。本文就细胞焦亡与脓毒症的关系及相关分子机制进行综述,以期为脓毒症的基础研究和未来治疗提供借鉴。

Sepsis is a life-threatening organ dysfunction that is caused by dysregulated host responses to infection.Sepsis or septic shock are one of the major causes of death among critically ill patients.Pyroptosis is defined as a specific programmed cell death characterized by release of inflammatory cytokines and cell swelling.Moderate pyroptosis in sepsis can alleviate bacterial infection and minimize tissue damage.However,excessive pyroptosis may aggravate sepsis or cause secondary infection.The activation of canonical or noncanonical inflammasomes,Gasdermin D,and pannexin-1 play important roles in the induction of pyroptosis.Therefore,this paper reviews the relationship between pyroptosis and sepsis,and summarizes the research progress of related molecular mechanisms.