Novel perspective in pancreatic cancer therapy: Targeting ferroptosis pathway

Figure 1 Metabolic mechanisms of ferroptosis in pancreatic ductal adenocarcinoma. A: Lipid metabolism; B: Iron metabolism[25]; C: Autophagy[26-28]; D: Amino acid metabolism[29-31]. ACSL4: Long-chain acyl-CoA synthetase 4; ALOXs: Arachidonate lipoxygenases; ATG5: Autophagy-related 5; ATG7: Autophagy-related 7; CoQ10: Coenzyme Q10; CoQ10H₂: Ubiquinol-10; DIAPH3: Diaphanous homolog 3; FSP1: Ferroptosis suppressor protein 1; GPX4: Glutathione peroxidase 4; GSH/GSSG: Glutathione; KEAP1: Kelch-like ECH-associated protein 1; LPCAT3: Lysophosphatidylcholine acyltransferase 3; LTF: Lactotransferrin; NAD(P)H: Nicotinamide adenine dinucleotide phosphate; NCOA4: Nuclear receptor coactivator 4; NEDD4L: Neural precursor cell-expressed developmentally downregulated 4-like; NRF2: Nuclear factor erythroid 2-related factor 2; P62/SQSTM1: Sequestosome 1; PIR: Pirin; PUFA: Polyunsaturated fatty acids; ROS: Reactive oxygen species; SLC3A2: Solute carrier family 3 member 2; SLC7A11: Solute carrier family 7 member 11; STEAP3: Six-transmembrane epithelial antigen of prostate 3; TF: Transferrin; TrxR1: Thioredoxin reductase 1.