Molecular Mechanisms of Pyroptosis
- PMID: 37074637
- DOI: 10.1007/978-1-0716-3040-2_1
Molecular Mechanisms of Pyroptosis
Abstract
Pyroptosis is a regulated form of cell death that leads to inflammation and plays a role in many different diseases. Pyroptosis was initially defined by the dependence on caspase-1, a protease which is activated by innate immune signaling complexes called inflammasomes. Caspase-1 cleaves the protein gasdermin D, releasing the N-terminal pore-forming domain, which inserts into the plasma membrane. Recent studies have revealed that other gasdermin family members form plasma membrane pores, leading to lytic cell death, and the definition of pyroptosis was revised to gasdermin-dependent cell death. In this review, we discuss how the use of the term pyroptosis has changed over time, as well as currently understood molecular mechanisms leading to pyroptosis and functional consequences of this form of regulated cell death.
Keywords: ASC; Gasdermin; Inflammasome; Macrophage; Pyroptosis; Regulated cell death.
© 2023. The Author(s), under exclusive license to Springer Science+Business Media, LLC, part of Springer Nature.
References
-
- Elmore S (2007) Apoptosis: a review of programmed cell death. Toxicol Pathol 35(4):495–516. https://doi.org/10.1080/01926230701320337 - DOI - PubMed - PMC
-
- Kerr JF, Wyllie AH, Currie AR (1972) Apoptosis: a basic biological phenomenon with wide-ranging implications in tissue kinetics. Br J Cancer 26(4):239–257. https://doi.org/10.1038/bjc.1972.33 - DOI - PubMed - PMC
-
- Fink SL, Cookson BT (2005) Apoptosis, pyroptosis, and necrosis: mechanistic description of dead and dying eukaryotic cells. Infect Immun 73(4):1907–1916. https://doi.org/10.1128/IAI.73.4.1907-1916.2005 - DOI - PubMed - PMC
-
- Julien O, Wells JA (2017) Caspases and their substrates. Cell Death Differ 24(8):1380–1389. https://doi.org/10.1038/cdd.2017.44 - DOI - PubMed - PMC
-
- Cookson BT, Brennan MA (2001) Pro-inflammatory programmed cell death. Trends Microbiol 9(3):113–114. https://doi.org/10.1016/s0966-842x(00)01936-3 - DOI - PubMed
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