| Cell death manner | Morphologic features | Biochemical characteristics | Key controlling genes | References |
| Ferroptosis | Membrane rupture or blistering, mitochondrial atrophy, crista reduction, lack of chromatin condensation | Lipid peroxidation in cells induced by ferrous or esterase | GPX4, p53, Ras, Nox, SLC7A11, TFR1 | [3, 4, 52] | Necrosis | Lipid peroxidation in cells induced by ferrous or esterase | Inflammatory response | ā | | Apoptosis | Cell membrane foaming, cell contraction, the formation of apoptotic bodies | DNA degradation | Bcl-2 family, caspase family, C-myc, p53 | [55, 56] | Autophagy | Cytoplasmic vacuolization to form autophagosomes | Increase activity of lysosomes | ATG5, ATG7, Beclin1 | [59, 199] | Necroptosis | Cell volume enlargement, organelle swelling, cell membrane perforation, with necrotic cell characteristics | Cell collapse, release contents, triggering an immune response, and clearing the dead cells through macropinocytosis bodies | RIPK1, RIPK3, TNFR1, caspase-8 | [66, 67] | Pyroptosis | Cell swelling, with a large number of bubble-like protrusions; a large number of vesicles, pyroptosis bodies, formed before the rupture of the plasma membrane | Formation of inflammatory bodies, activation of caspase and gasdermin, the release of a large number of proinflammatory factors | Caspase family, NLRP3, ASC | [71ā73] |
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