Table 1.

Comparison of Characteristics of Apoptosis, Necrosis, Pyroptosis and Ferroptosis.

	Definitions	Morphological features	Biochemical features
Apoptosis	Type of RCD initiated by perturbation of the extracellular or intracellular microenvironment; Demarcated by mitochondrial outer membrane permeabilization (MOMP); Precipitated by executioner caspases, mainly caspase3 (CASP3).	Rounding-up of the cell; Retraction of pseudopods; Reduction of cellular and nuclear volume (pyknosis); Nuclear fragmentation (karyorrhexis); Minor modification of cytoplasmic organelles; Plasma membrane blebbing; Engulfment by resident phagocytes in vivo.	Release of mitochondrial intermembrane space ‘IMS’ proteins; Respiratory chain inhibition.
MTP-driven Necrosis	Specific form of RCD triggered by perturbations of the intracellular microenvironment and relying on cyclophilin D (CYPD).	Rupture of plasma Membrane; Cytoplasm: cytoplasmic swelling. (Oncosis): Swelling of cytoplasmic organelles; Moderate chromatin condensation.	Caspase inhibition; NADPH oxidase activation; Neutrophil extracellular traps (NETs) release (in some instances).
Pyroptosis	A type of RCD that critically depends on the formation of plasma membrane pores by members of the gasdermin protein family; Often (but not always) as a consequence of inflammatory caspase activation.	The early membrane rupture of pyroptotic cells exposes the inner leaflet of the plasma membrane to the extracellular surface; Transmembrane ion fluxes; Cytoplasmic swelling; Osmotic lysis of the cell.	Caspase-1 activation; Caspase-7 activation; Secretion of IL-1β and IL18.
Ferroptosis	A form of RCD initiated by oxidative perturbations of the intracellular microenvironment that is under constitutive control by GPX4 and can be inhibited by iron chelators and lipophilic antioxidants.	Normal nuclei and shrinking mitochondria that show increased membrane density and outer mitochondrial membrane rupture.	Iron and ROS accumulation; Inhibition of system xc−; With decreased cystine uptake; GSH depletion and increased; NAPDH oxidation Release of arachidonic acid mediators.