Fig. 4: Mechanisms of cellular oxeiptosis, disulfidptosis, autophagy and paraptosis.

a Schematic diagram of the oxeiptosis pathway. After being phosphorylated, AIFM1 in mitochondria is translocated to the nucleus under the action of PGAM5, where it causes DNA damage and ultimately leads to cell death. This process is regulated by KEAP1. b Schematic diagram of the disulfidptosis pathway. Under glucose-deprivation conditions, the supply of NADPH becomes limited, leading to excessive accumulation of cysteine and other disulfide-containing molecules in SLC7A11-high cells. This ultimately induces a disulfide stress state, which triggers rapid disulfide-dependent cell death. c Schematic diagram of the autophagy pathway. Nutrients and insulin signals can activate mammalian targets of mTOR. DDIT4-AS1 can inhibit mTOR, thereby activating ULK1 and promoting the formation of autophagosomes. In addition, H19 can affect the autophagy process by regulating SAHH and DNMT3B or through the HER2/HuR/LINC00969/trastuzumab axis. d Schematic diagram of the paraptosis pathway. Endoplasmic reticulum stress leads to Ca²⁺ depletion and the accumulation of misfolded proteins. Mitochondrial dysfunction causes Ca²⁺ overload and ROS generation, resulting in mitochondrial vacuolisation and ultimately cell death mediated by AIP-1/Alix. MANF: Neurotrophic factor; MAPK: Mitogen-activated protein kinase. AIFM1: Apoptosis-inducing factor mitochondrial 1; P: Phosphorylated; PGAM5: Phosphoglycerate mutase 5; PPP: Pentose phosphate pathway; NADPH: Nicotinamide adenine dinucleotide phosphate; NADP⁺: Nicotinamide adenine dinucleotide phosphate; Ca²⁺: Calcium ion; ROS: Reactive oxygen species. The figure was created with BioRender.com.