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细胞焦亡在病毒感染中的作用。

The role of pyroptosis in viral infection.

机构信息

Department of Pathogenic Biology, School of Basic Medicine, Qingdao University, Qingdao, 266071, China.

Department of Clinical Laboratory, Zibo Central Hospital, Zibo, 255036, China.

出版信息

Arch Virol. 2024 Mar 8;169(3):69. doi: 10.1007/s00705-024-05978-9.

Abstract

Pyroptosis, also known as inflammatory necrosis, is a form of programmed cell death, which is an important natural immune response. Pyroptosis plays a major role in combating pathogenic infections. The mechanism of pyroptosis is distinct from other forms of cell death and is characterized by its dependence on inflammatory caspases (mainly caspases 1, 4, 5, and 11). Activation of NOD-like receptor thermal protein domain associated protein 3 (NLRP3) inflammatory vesicles is involved in caspase-1 activation and cleavage, which in turn triggers cleavage and multimerization of multiple gasdermin family members, including gasdermin-D (GSDMD). This further leads to cell perforation and cellular distension, causing cell membrane rupture, resulting in a massive efflux of cell contents, which triggers inflammatory reactions. In recent years, detailed study of viral diseases, has demonstrated that pyroptosis is closely associated with the development of viral diseases. This article focuses on the mechanism of pyroptosis and the connection between pyroptosis and viral infection.

摘要

细胞焦亡,又称炎症性细胞坏死,是一种程序性细胞死亡方式,也是一种重要的天然免疫反应。细胞焦亡在抵抗病原感染中发挥重要作用。细胞焦亡的发生机制有别于其他形式的细胞死亡,其特征为依赖于炎性半胱天冬酶(主要是半胱天冬酶 1、4、5 和 11)。NOD 样受体热蛋白结构域相关蛋白 3(NLRP3)炎性小体的激活涉及半胱天冬酶-1 的激活和切割,进而触发多种 Gasdermin 家族成员(包括 Gasdermin-D[GSDMD])的切割和多聚化。这进一步导致细胞穿孔和细胞膨胀,引起细胞膜破裂,导致大量细胞内容物外流,引发炎症反应。近年来,对病毒性疾病的详细研究表明,细胞焦亡与病毒性疾病的发生发展密切相关。本文聚焦于细胞焦亡的发生机制以及细胞焦亡与病毒感染之间的关系。

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