细胞焦亡:病原体感染过程中的双刃剑综述

Pyroptosis, a double-edged sword during pathogen infection: a review.

作者信息

Zhang Yuanhang, Zhao Dengshuai, Wang Tianyu, Li Ping, Yu Dixi, Gao Han, Zhao Mengmeng, Qin Limei, Zhang Keshan

机构信息

Guangdong Provincial Key Laboratory of Animal Molecular Design and Precise Breeding, School of Animal Science and Technology, Foshan University, Foshan, 528225, China.

College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, 210095, China.

出版信息

Cell Death Discov. 2025 Jul 1;11(1):289. doi: 10.1038/s41420-025-02579-6.

Abstract

Pyroptosis, a distinctive form of programmed cell death (PCD) characterized by its inflammatory nature, is triggered by the activation of pore-forming proteins known as gasdermins (GSDMs). This process is marked by progressive expansion of a pore within the cell, ultimately leading to cellular membrane disruption and the substantial release of intracellular contents. Pyroptosis plays a pivotal role in the eradication of intracellular pathogen replication niches and in the modulation of the immune system through the release of danger signals. Emerging evidence suggests that viruses have developed sophisticated strategies to evade immune surveillance and establish persistent infections by manipulating host pyroptotic pathway This review presents recent advances on the mechanisms by which two major pathogens (virus and bacteria) activate or inhibit the pyroptosis process through their effector proteins, thereby facilitating their dissemination and blocking host immunity. These insights provide new perspectives on the regulatory mechanisms of interactions between hosts and pathogens in the pyroptosis process.

摘要

细胞焦亡是一种独特的程序性细胞死亡(PCD)形式,其特点是具有炎症性质,由称为gasdermin(GSDM)的成孔蛋白激活所触发。这个过程的标志是细胞内的孔逐渐扩大,最终导致细胞膜破裂和细胞内内容物大量释放。细胞焦亡在消除细胞内病原体复制位点以及通过释放危险信号调节免疫系统方面发挥着关键作用。新出现的证据表明,病毒已经发展出复杂的策略来逃避免疫监视,并通过操纵宿主细胞焦亡途径建立持续性感染。本综述介绍了两种主要病原体(病毒和细菌)通过其效应蛋白激活或抑制细胞焦亡过程的机制的最新进展,从而促进它们的传播并阻断宿主免疫。这些见解为细胞焦亡过程中宿主与病原体相互作用的调节机制提供了新的视角。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f7fa/12217603/0163fae0918f/41420_2025_2579_Fig1_HTML.jpg

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