Table 1 Type of cell death

Autophagy

Removes abnormal proteins and organelles and maintains cell homeostasis by removing misfolded proteins and damaged organelles and invading microorganisms through lysosomes

A large vacuole of the cytoplasm, the formation of autophagosomes, phagocytosis and subsequent lysosomal degradation

Infection; immune disease; metabolic disease; cancer; neurodegenerative

[27, 28]

Apoptosis

Citing no inflammatory responses regulated by genes, which plays important roles in maintain cells stability in tissues, immune and defense responses, growth and development of tumors, and cells damage caused by poisoning

The contraction of cytoplasm, shrinkage of the nucleus, rupture of the nucleus, fragmentation of DNA, foaming of plasma membranes, and formation of apoptosis bodies

Cancer; atherosclerosis, diabetes; hepatic fibrosis; wound healing

[29, 30]

Necroptosis

A type of regulated necrosis that critically depends on RIPK3 and MLKL

Organelles and plasma membrane rupture, and the final treated cell cadavers were not obviously involved in phagocytes and lysosomes

Viral infection; acute kidney injury; cardiac ischemia/reperfusion; human tumors

[31]

Ferroptosis

A form of cell death driven by iron-dependent lipid peroxidation

Genetics

Regulated by multiple genes, mainly the changes of iron homeostasis and lipid peroxidation genes

Aging; immunity; cancer; cardiovascular diseases; ischemic-reperfusion

[32, 33]

Morphology

The mitochondrial volume decreased, the density of double-layer structure increased, the crest decreased or disappeared

Immunology

Injury-related molecular pattern molecules release inflammatory mediators to trigger inflammatory response

Biochemistry

GSH consumption, GPX4 activity decreased, Fe²⁺ mediated lipid peroxidation through Fenton reaction, produce excess ROS

Cuproptosis

Copper directly binds to lipoylated components of the tricarboxylic acid (TCA) cycle, causing protein aggregation, iron-sulfur cluster protein loss, proteotoxic stress, and cell death

The key regulators:

FDX1 and protein lipoylation

Wilson’s; Alzheimer's disease; Parkinson's disease

[34,35,36]

Function channel:

Mitochondrial respiration

Upstream regulator

FDX1

Pyroptosis

A form of programmed cell death mediated by the N-terminal fragment of gasdermin D that gives rise to inflammation via the release of some proinflammatory cytokines, including IL-1β, IL-18 and HMGB1

The canonical signalling pathway dependent on caspas-1 and the non-canonical signalling pathway determined by caspas-4/5/11

Fibrosis; Kidney disease; atherosclerosis; diabetes; neurodegenerative diseases;

[37,38,39,40]