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Fig. 1 | Biomarker Research

Fig. 1

From: Effect of regulatory cell death on the occurrence and development of head and neck squamous cell carcinoma

Fig. 1

Core molecular mechanisms of apoptosis, necroptosis, pyroptosis, ferroptosis, autophagy and cuproptosis. A In the exogenous apoptosis pathway, TNF interacts with TNFR1, and TNFR1 begins to recruit downstream protein molecules to form complexes I and IIa, which promote the activation of caspase-8 and then activate caspase-3 and caspase-7. In the endogenous apoptotic pathway, activation of BH3-only proteins leads to Bax and BAK activity, triggering MOMP. Cyto C is released from mitochondria and forms a multiapoptotic complex with APAF1, which activates caspase-9 and then caspase-3 and caspase-7, leading to apoptosis. B TNF interacts with TNFR1; when caspase 8 is inhibited, activated RIPK1 promotes RIPK3 recruitment and MLKL phosphorylation, forms complex IIb, promotes inflammatory signal secretion, and promotes necroptosis. C PAMP and DAMP stimulate inflammasome activation, which leads to caspase-1 cleavage, and LPS can bind to caspase-4/5/11 to lyse GSDMD. Potassium efflux triggers the release of HMGB1 and K+. Caspase-3 can also be activated through the mitochondrial endogenous pathway and death receptor pathway to lyse GSDME and trigger pyroptosis. D Iron accumulation is achieved by increasing iron uptake by the TF-TFRC complex, limiting iron efflux by iron export transporters, and reducing iron storage by ferritosis. Cells obtain cysteine and exchange it for glutamate through the XC − antitransporter system. The ACSL4-LPCAT3-AlOXs pathway promotes iron death by activating lipid peroxidation to produce PLOOH from polyunsaturated fatty acids. E AMPK and mTORC1 act on mTOR, the ULK1 complex is phosphorylated, and the PI3K complex interacts with autophagosomes. Lc3 is modified to form LC3-II and ATG5-ATG12-ATG16L complexes to promote the formation and maturation of autophagic vesicles and binds to lysosomes under the action of LAMP, Rab7 and VAMP7. The recovered product is released into the cytosol for reuse. F Elesclomol binds extracellular copper (Cu2+) and transports it into the cell. FDX1 reduces Cu2 + to Cu + and promotes lipolylation (LA) and aggregation of DLAT involved in the mitochondrial TCA cycle. Copper importers (e.g., SLC31A1) and exporters (e.g., ATP7B) modulate copper sensitivity by affecting intracellular copper ion levels

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