上睑下垂
炎症
发病机制
蛋白酵素
先天免疫系统
败血症
半胱氨酸蛋白酶1
程序性细胞死亡
免疫系统
医学
细胞生物学
生物
免疫学
细胞凋亡
炎症体
生物化学
酶
作者
Swathy O. Vasudevan,Bharat Behl,Vijay Rathinam
标识
DOI:10.1016/j.smim.2023.101781
摘要
Pyroptosis is a programmed necrotic cell death executed by gasdermins, a family of pore-forming proteins. The cleavage of gasdermins by specific proteases enables their pore-forming activity. The activation of the prototype member of the gasdermin family, gasdermin D (GSDMD), is linked to innate immune monitoring by inflammasomes. Additional gasdermins such as GSDMA, GSDMB, GSDMC, and GSDME are activated by inflammasome-independent mechanisms. Pyroptosis is emerging as a key host defense strategy against pathogens. However, excessive pyroptosis causes cytokine storm and detrimental inflammation leading to tissue damage and organ dysfunction. Consequently, dysregulated pyroptotic responses contribute to the pathogenesis of various diseases, including sepsis, atherosclerosis, acute respiratory distress syndrome, and neurodegenerative disorders. This review will discuss the inflammatory consequences of pyroptosis and the mechanisms of pyroptosis-induced tissue damage and disease pathogenesis.
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