炎性小体激活与细胞焦亡在急性胰腺炎中的研究进展
Research progress of inflammasome activation and pyrodeath in acute pancreatitis
王烁 1郑平 1鲁兵 1张桂英2
作者信息
- 1. 湘雅常德医院消化内科,湖南 常德 415000
- 2. 中南大学湘雅医院消化内科
- 折叠
摘要
急性胰腺炎(acute pancreatitis,AP)是一种发病率和死亡率高的非感染性炎症性疾病,主要表现为胰腺炎症和组织坏死.近年来发现的一种新的依赖半胱天冬氨酸蛋白酶(Caspase)的并由 gasdermin 介导的程序性细胞死亡方式—细胞焦亡(pyroptosis),区别于经典的细胞凋亡和坏死介导的细胞死亡概念,其是由细胞肿胀和膜变性引起,导致细胞成分大量分泌和炎症反应.炎性小体在细胞焦亡的过程中发挥着至关重要的作用.细胞感染或细胞应激能够激活炎性小体,导致炎性小体多蛋白复合物组装、Caspase-1 激活及其下游底物和 GSDMD、IL-1β前体及 IL-18 前体活化成熟,从而参与机体的免疫炎性反应及诱导细胞焦亡发生.近年来,越来越多的证据表明炎性小体的激活及细胞焦亡在 AP 的发生发展中起关键作用.
Abstract
Acute pancreatitis(AP)is a noninfectious inflammatory disease characterized by pancreatitis and tissue necrosis with high morbidity and mortality.In recent years,a new gasdermin-mediated programmed cell death mode de-pendent on caspase proteases,pyroptosis,has been discovered,which is different from the classical concepts of apopto-sis and necrosis mediated cell death,which is caused by cell swelling and membrane degeneration.Resulting in the se-cretion of cellular components and inflammatory response.The inflammasome plays an important role in the process of pyrodeath.Cell infection or cell stress can activate inflammasome,leading to inflammasome multi-protein complex as-sembly,caspase-1 activation and activation and maturation of its downstream substrates and GSDMD,IL-1β precursors and IL-18 precursors,thus participating in immune inflammatory response and inducing pyrodeath.In recent years,more and more evidence shows that inflammasome activation and pyroptosis play a key role in the occurrence and devel-opment of AP.
关键词
细胞焦亡/炎性小体/急性胰腺炎Key words
Pyroptosis/Inflammasome/Acute pancreatitis引用本文复制引用
出版年
2024
NETL
NSTL
万方数据