TABLE 1.

The comparative study of different types of cell death.

Type of cell death	Morphological features	Biochemical features	Regulatory genes
Ferroptosis	Rupture of the cell membrane; reduction and morphological shrinkage of mitochondria; an increase in density of bilayer membrane structure; reduction or disappearance of mitochondrial cristae	Decrease in GPX4 activity; iron overload; depletion of glutathione; accumulation of ROS	GPX4, SLC7A11, Nrf2, p53, ACSL4, FSP1	Hirschhorn and Stockwell, (2019)
Autophagy	Autophagy body and autophagic lysosomes formation	Microautophagy is mediated by direct lysosomal engulfment of cytoplasmic cargo. Chaperone-mediated autophagy through heat shock proteins recognizes particular proteins and degrades in lysosomes. Macroautophagy is the fusion of autophagy bodies and lysosomes	RIP1, RIP3, PI3K, p53, ATG	Glick et al. (2010)
Apoptosis	Blebbing of the plasma membrane, cell rounding; decrease of cellular and nuclear volume; DNA cleavage; nuclear fragmentation, chromatin condensation; formation of apoptotic bodies	Mitochondrial outer membrane permeabilization through the intrinsic pathway, the extrinsic pathway, and the endoplasmic reticulum pathway	Caspases, Bcl-2 family proteins, TNF-α, Fas, p53	Wang et al. (2015); Bertheloot et al. (2021)
Necrosis	Increased cell membrane permeability, cell swelling; organelle deformation or swelling; plasma membrane rupture; chromatin condensation; cell component overflow	Decrease in ATP level through RIP3-MLKL related signaling pathways, PKC-MAPK-AP-1 related signaling pathway, ROS-related metabolic regulation pathway	PIPK3, ATG5, ATG7, Caspase-8, Beclin-1	Tonnus et al. (2019)
Pyroptosis	The cells swelled and expanded, and many bubbles like protrusions form; scorched bodies form; the cell membrane breaks and the content flows out	The formation of inflammatory bodies; the activation of inflammatory caspases gasdermin; the release of a mass of proinflammatory factors	Caspase-1/11, IL-18	Yu et al. (2021a); Bertheloot et al. (2021)
Cuproptosis	Reduction of mitochondria volume and cristae; increased density of bilayer membrane structure	Excessive Cu accumulation triggers disruption of iron-sulfur cofactors; stimulates harmful reactive oxygen species resulting from Fenton reactions; Cu-dependent, mitochondria-induced cell death	Lipoylation DLAT, PDHA1, PDHB, SLC25A3, FDX1, LIAS, HSP70	Wang et al. (2022a)