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Gasdermins: Effectors of Pyroptosis
Stephen B Kovacs1, Edward A Miao1
1Department of Microbiology and Immunology, Lineberger Comprehensive Cancer Center, and Center for Gastrointestinal Biology and Disease, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
Trends in Cell Biology
|June 17, 2017
Summary
Pyroptosis, a lytic cell death, is triggered by inflammasomes and executed by gasdermins forming membrane pores. This review covers pyroptosis mechanisms and the gasdermin protein family.
Area of Science:
- Cellular Biology
- Immunology
Background:
- Pyroptosis is a programmed lytic cell death pathway.
- It is initiated by inflammasomes sensing cellular danger signals.
Purpose of the Study:
- To review the current understanding of pyroptosis.
- To summarize knowledge of the gasdermin protein family.
Main Methods:
- Review of existing literature on pyroptosis and gasdermins.
- Analysis of inflammasome activation pathways.
- Examination of gasdermin family members and their functions.
Main Results:
- Inflammasomes activate caspases (e.g., caspase-1, caspase-11) that cleave gasdermin D.
- Cleavage separates the pore-forming domain, leading to membrane rupture and cell lysis.
- Other gasdermins, like gasdermin E, can also mediate pyroptosis upon cleavage (e.g., by caspase-3).
Conclusions:
- Gasdermin proteins are key effectors of pyroptosis.
- Understanding pyroptosis and gasdermins is crucial for studying inflammatory diseases and cell death.
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