Fig. 2: Comparison of the main processes leading to DAMP release in apoptosis, necroptosis, pyroptosis and ferroptosis.
From: Types of necroinflammation, the effect of cell death modalities on sterile inflammation
During apoptosis, caspase-regulated events lead to the wrapping of intracellular components into apoptotic bodies. Subsequent efferocytosis prevents the release of DAMPs into the extracellular space. Necrosome induction results in the activation of cation-selective ion channels, leading to cell lysis due to osmotic shock. Pyroptosis is characterized by the secretion of IL-1 and IL-18 cytokines by inflammasome activation and the formation of voluminous non-selective pores formed by GSDMs. In ferroptosis, oxidative perturbations accumulate toxic lipid peroxides that ultimately cause the DAMP release. PRR Pattern Recognition Receptor DR death receptor, GSDM gasdermin, ADAM a disintegrin and metalloproteinase, TRPM7 Transient receptor potential cation channel, subfamily M, member 7, 4HNE 4-Hydroxynonenal, PGE2 Prostaglandin E2, OX PLS oxidized glycerophospholipids, LTB4 Leukotriene B4, LTC4 Leukotriene C4, LTD4 Leukotriene D4, RIPK1 Receptor-interacting serine/threonine-protein kinase, MLKL Mixed lineage kinase domain-like pseudokinase.
