When cell death goes wrong: inflammatory outcomes of failed apoptosis and mitotic cell death

被引:31
作者
Bock, Florian J. [1 ]
Riley, Joel S. [2 ]
机构
[1] Maastricht Univ, GROW Sch Oncol & Reprod, Dept Radiat Oncol Maastro, Med Ctr, Maastricht, Netherlands
[2] Med Univ Innsbruck, Inst Dev Immunol, BioCtr, Innsbruck, Austria
关键词
NF-KAPPA-B; TRIGGER NLRP3 INFLAMMASOME; MITOCHONDRIAL-DNA RELEASE; CYTOCHROME-C; CANCER-CELLS; FIND-ME; EXTRINSIC APOPTOSIS; FAS LIGAND; TNF-ALPHA; CASPASE-8;
D O I
10.1038/s41418-022-01082-0
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Apoptosis is a regulated cellular pathway that ensures that a cell dies in a structured fashion to prevent negative consequences for the tissue or the organism. Dysfunctional apoptosis is a hallmark of numerous pathologies, and treatments for various diseases are successful based on the induction of apoptosis. Under homeostatic conditions, apoptosis is a non-inflammatory event, as the activation of caspases ensures that inflammatory pathways are disabled. However, there is an increasing understanding that under specific conditions, such as caspase inhibition, apoptosis and the apoptotic machinery can be re-wired into a process which is inflammatory. In this review we discuss how the death receptor and mitochondrial pathways of apoptosis can activate inflammation. Furthermore, we will highlight how cell death due to mitotic stress might be a special case when it comes to cell death and the induction of inflammation.
引用
收藏
页码:293 / 303
页数:11
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