Morphological Changes
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Cell shrinkage.
Maintenance of the integrity of the plasma membrane.
Formation of membrane blebs.
Degradation of genomic DNA.
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Cellular enlargement and subsequent rupture.
Breakdown of the plasma membrane.
Breakage of DNA.
Generation of pores in the plasma membrane.
Maintenance preservation of nuclear integrity.
Occurrence of nuclear condensation.
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Molecular Mechanism
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Absence of an inflammatory reaction.
Generation of apoptosome and liberation of Cytochrome-C.
Activation of Caspases 8, 9, 3, 6, and 7.
Activation of pro-apoptotic BCL-2 and DISC proteins.
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Inflammatory cell death.
Development of an inflammasome and activation of gasdermins.
Activation of interleukin-1β (IL-1β) and interleukin-18 (IL-18).
Activation of GSDME and NLRP3 inflammasome, via canonical and non-canonical routes.
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Regulation
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The apoptotic cell death occurs when the ubiquitination of RIPK1 is inhibited, leading to the formation of a complex between RIPK1, FADD, and pro-caspase-8. This complex activates caspase-8, which then cleaves RIPK1, ultimately resulting in the apoptotic cell death. |
NLRP3 and other proteins are regulated by post-translational phosphorylation and ubiquitylation modifications. |
Mitochondrial Participation
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The release of Cytochrome-C from mitochondria and the subsequent generation of apoptotic bodies. |
Mitochondria are engaged in the control of gasdermin D oligomerization and the consequent development of pores in the plasma membrane. |