Table 1 Comparison between pyroptosis, apoptosis, necroptosis, and ferroptosis

Inducing factors

ICD, Microbial infection, DAMPs, PAMPs,

TNF-α, FasL, TRAIL, Irradiation, Hypoxia, Heat shock

TNF-α, FasL, TRAIL, Pathogenic infection

Fe²⁺ overload initiation and ROS generation

Biochemical events

Assembly of inflammasome, Caspase-dependent GSDM cleavage, IL-18 and IL-1β release

HSPs, P53, Bcl-2 protein, cytochrome c release, formation of DISC, initiator/effector caspase cascade

RIPK1/RIPK3-mediated phosphorylation of MLKL, permeabilization of the lysosomal membrane, mitochondrial damage

iron accumulation, peroxidation of PUFAs, inhibition of Xc-system/GSH/GPX4

Cell morphology

Cells swelling, pore formation, rupture and bubbling of plasma membranes, Nucleus intact, Chromatin condensation, DNA fragmentation

Cell and nuclear volume reduced, Membrane intact, Formation of apoptotic bodies, Chromatin condensation, DNA fragmentation

Cells swelling, pore formation, rupture of plasma membranes, Cytoplasmic and organelle swelling, chromatin condensation

Cells swelling, pore formation, decreased mitochondria crista, Condensed mitochondrial membrane, Rupture of mitochondrial outer membrane

Cell release

Cellular content, DAMPs (IL-18, IL-10, IL-1β, HMGB1, ATP, dsDNA)

Usually no release, In certain cases: DAMPs (HMGB1, ATP, dsDNA, calreticulin)

Cellular content, DAMPs (IL-1α, IL-33, IL-6, HMGB1, ATP, HSPs)

DAMPs (KRAS-G12D, HMGB1, 8-OHG, and PGE2)

Inflammatory response

Yes

No

Yes

Yes

References

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