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Trends Biochem Sci. 2017 Apr;42(4):245-254. doi: 10.1016/j.tibs.2016.10.004. Epub 2016 Dec 5.

Pyroptosis: Gasdermin-Mediated Programmed Necrotic Cell Death.

Author information

1
National Institute of Biological Sciences, Number 7 Science Park Road, Zhongguancun Life Science Park, Beijing 102206, China.
2
National Institute of Biological Sciences, Number 7 Science Park Road, Zhongguancun Life Science Park, Beijing 102206, China. Electronic address: shaofeng@nibs.ac.cn.

Abstract

Pyroptosis was long regarded as caspase-1-mediated monocyte death in response to certain bacterial insults. Caspase-1 is activated upon various infectious and immunological challenges through different inflammasomes. The discovery of caspase-11/4/5 function in sensing intracellular lipopolysaccharide expands the spectrum of pyroptosis mediators and also reveals that pyroptosis is not cell type specific. Recent studies identified the pyroptosis executioner, gasdermin D (GSDMD), a substrate of both caspase-1 and caspase-11/4/5. GSDMD represents a large gasdermin family bearing a novel membrane pore-forming activity. Thus, pyroptosis is redefined as gasdermin-mediated programmed necrosis. Gasdermins are associated with various genetic diseases, but their cellular function and mechanism of activation (except for GSDMD) are unknown. The gasdermin family suggests a new area of research on pyroptosis function in immunity, disease, and beyond.

KEYWORDS:

caspase; gasdermin; innate immunity; necrosis; pore-forming protein; pyroptosis

PMID:
27932073
DOI:
10.1016/j.tibs.2016.10.004
[Indexed for MEDLINE]

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