Emerging connectivity of programmed cell death pathways and its physiological implications

被引:645
作者
Bedoui, Sammy [1 ]
Herold, Marco J. [2 ,3 ]
Strasser, Andreas [2 ,3 ]
机构
[1] Univ Melbourne, Doherty Inst Infect & Immun, Dept Microbiol & Immunol, Parkville, Vic, Australia
[2] Walter & Eliza Hall Inst Med Res, Parkville, Vic, Australia
[3] Univ Melbourne, Dept Med Biol, Parkville, Vic, Australia
基金
英国医学研究理事会;
关键词
NF-KAPPA-B; C-MYC; INFLAMMATORY CASPASES; APOPTOTIC RESPONSES; NLRP3; INFLAMMASOME; ESSENTIAL MEDIATOR; PSEUDOKINASE MLKL; AIM2; MOLECULAR SWITCH; BCL-2; INHIBITORS;
D O I
10.1038/s41580-020-0270-8
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Dispensable, infected or neoplastic cells are removed by programmed cell death, including pathways for apoptosis, necroptosis and pyroptosis. Owing to differences in their mechanisms and physiological outcomes, these cell death pathways have traditionally been viewed as separate entities, but it has become clear that they are mechanistically and functionally connected. The removal of functionally dispensable, infected or potentially neoplastic cells is driven by programmed cell death (PCD) pathways, highlighting their important roles in homeostasis, host defence against pathogens, cancer and a range of other pathologies. Several types of PCD pathways have been described, including apoptosis, necroptosis and pyroptosis; they employ distinct molecular and cellular processes and differ in their outcomes, such as the capacity to trigger inflammatory responses. Recent genetic and biochemical studies have revealed remarkable flexibility in the use of these PCD pathways and indicate a considerable degree of plasticity in their molecular regulation; for example, despite having a primary role in inducing pyroptosis, inflammatory caspases can also induce apoptosis, and conversely, apoptotic stimuli can trigger pyroptosis. Intriguingly, this flexibility is most pronounced in cellular responses to infection, while apoptosis is the dominant cell death process through which organisms prevent the development of cancer. In this Review, we summarize the mechanisms of the different types of PCD and describe the physiological and pathological processes that engage crosstalk between these pathways, focusing on infections and cancer. We discuss the intriguing notion that the different types of PCD could be seen as a single, coordinated cell death system, in which the individual pathways are highly interconnected and can flexibly compensate for one another.
引用
收藏
页码:678 / 695
页数:18
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