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. 2024 Jul 31;14:1416819. doi: 10.3389/fcimb.2024.1416819

Table 1.

Programmed cell death pathways with their morphological and biochemical features.

Programmed cell death Morphological features and key pathway components References
Apoptosis Nuclear and cytoplasmic condensation (pyknosis), formation of extracellular vesicles (apoptotic bodies) and phagocytosis by surrounding cells.
Pro-apoptotic proteins of the BCL-2 family, MOMP, caspase activation (e.g. Apaf-1 in intrinsic apoptosis or FADD in extrinsic apoptosis), cleavage of caspase substrates and ROS production.
(Kerr et al., 1972)

(Li et al., 1997)
(Stennicke et al., 1998)
Necroptosis Cell swelling, rupture of the plasma membrane, swelling of the cytoplasmic organelles and release of intracellular contents.

Inhibition of caspase-8, activation of RIPK1 and RIPK3, formation of the necrosome complex, phosphorylation of MLKL, inflammatory response and release of DAMPs (also called PAMPs in pathogenically infected cells).
(Degterev et al., 2005)


(Li and Beg, 2000)
(Holler et al., 2000)
Pyroptosis Cell swelling or lack of cell swelling, rupture of the plasma membrane and release of intracellular contents (inflammation-related).


Activation of the inflammasome, cleavage of the GSDMD protein, release of pro-inflammatory cytokines (e.g. IL-18).
(Cookson and Brennan, 2001)
(Moujalled et al., 2021)

(Galluzzi et al., 2018)
Autophagy Vacuolization of the cytoplasm, formation of autophagosomes, without chromatin condensation.

ATG family proteins and the conversion of LC3-I to LC3-II (e.g. ATG7 and ATG3 are involved in the phosphorylation and lipidation of LC3 and promote the conversion).
(Mizushima and Komatsu, 2011)
(Bergmann, 2007)
Ferroptosis Mitochondria that appear smaller than normal, with increased membrane density.

Excessive accumulation of iron, peroxidation of membrane lipids and glutathione depletion.
(Dixon et al., 2012)

(Stockwell, 2022)

B-cell lymphoma gene 2 (BCL-2), Mitochondrial outer membrane permeabilization (MOMP), Apoptotic peptidase activating factor 1 (Apaf-1), FAS-associated death domain (FADD), Reactive oxygen species (ROS), Receptor-interacting serine/threonine-protein kinase 1 (RIPK1) activation, Mixed lineage kinase domain-like protein (MLKL), Damage-associated molecular patterns (DAMPs), Gasdermin D (GSDMD), Interleukin-18 (IL-18), Autophagy-related protein (ATG), Microtubule-associated protein 1A/1B-light chain 3 (LC3).