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Review
. 2018 Dec;34(6):1131-1136.
doi: 10.1007/s12264-018-0294-7. Epub 2018 Oct 10.

The Possibility and Molecular Mechanisms of Cell Pyroptosis After Cerebral Ischemia

Affiliations
Review

The Possibility and Molecular Mechanisms of Cell Pyroptosis After Cerebral Ischemia

Zhaofei Dong et al. Neurosci Bull. 2018 Dec.
No abstract available

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Conflict of interest statement

The authors claim no conflicts of interest.

Figures

Fig. 1
Fig. 1
Pyroptosis pathways. In the canonical inflammasome pathway, microbial pathogens (PAMPs) or sterile inflammatory substances (DAMPs) are detected by various cytosolic sensor proteins (PRRs) which leads to caspase-1 activation through an inflammasome complex. Active caspase-1 converts the precursors of IL-1β and IL-18 to their mature forms, which are released from cells by pyroptosis. In the non-canonical pathway, LPS in the cytosol of cells infected by bacteria binds to precursor caspase-4/5/11, which leads to the activation of caspase-4/5/11. Both caspase-1 and caspase-4/5/11 process GSDMD, which results in the release of the N-terminal fragment of GSDMD (GSDMD-N). GSDMD-N forms pores in the plasma membrane that induce pyroptosis. The other pathway of pyroptosis is caspase-3/GSDME (DFNA5). Caspase-3 can be activated by the mitochondrial pathway and the death receptor pathway. Activated caspase-3 in turn cleaves GSDME to generate the GSDME-N fragment that forms pores in the plasma membrane and induces secondary necrosis/pyroptosis [1]. PAMPs pathogen-associated molecular patterns; DAMPs danger-associated molecular patterns; PRRs pattern recognition receptors; ASC apoptosis-associated speck-like protein containing a CARD; LPS lipopolysaccharide; GSDMD gasdermin D; GSDME (DFNA5), gasdermin E (deafness autosomal dominant type 5).

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