Figure 1.

The mechanism of ferroptosis. The figure shows the related molecules and pathways of ferroptosis. Ferroptosis is caused by the inhibition of the system Xc⁻/GSH/GPX4 axis or the accumulation of Fe²⁺ and lipid peroxidation. Regulators of iron metabolism, including TF, TFR1, and ferritinophagy, regulate ferroptosis by enhancing the labile iron pool-mediated Fenton reaction, and FSP1 can negatively regulate ferroptosis through CoQ10, thereby inhibiting the delivery of lipid peroxides. Abbreviations: ACSL4, acyl-CoA synthetase long-chain family member 4; DMT1, divalent metal transporter 1; FSP1, ferroptosis suppressor protein; GPX4, glutathione peroxidase 4; GR, glutathione-disulfide reductase; GSH, glutathione; GSS, GSH synthetase; GSSG, oxidized glutathione; IREB2, iron responsive element binding protein 2; LPCAT3, lysophosphatidylcholine acyltransferase 3; PUFAs, polyunsaturated fatty acids; STEAP3, six transmembrane epithelial antigen of prostate 3; SLC3A2, solute carrier family 3 member 2; SLC7A11, solute carrier family 7 member 11; TF, transferrin; TFR1, transferrin receptor 1; ZIP8/14, zinc/iron regulatory protein family 8/14. PUFA-PL*, polyunsaturated fatty acid-phospholipid radical; PUFA-PL-OO*, polyunsaturated fatty acid-phospholipid ethanolamine peroxyl radical. Black arrows indicate the activation modification, and red block lines indicate inhibitory modification. Black dashed arrows indicate the indirect process. Double arrows indicate the reverse transport process of glutamate and cystein.