Fig. 1.

Molecular regulating mechanisms of ferroptosis. Ferroptosis is mainly driven by PUFL-PLs synthesis and features abnormal iron accumulation, diminished mitochondrial cristae, and rupture of the cell membrane. The synthesis of PUFL-PLs attributes to three perspectives: iron toxicity through the Fenton reaction; transduction of polyunsaturated fatty acids (PUFAs); iron metabolism and ROS metabolism in the mitochondrion. Meanwhile, ferroptosis occurs when oxidation-promoting activities surpass the detoxification capabilities or the antioxidant system is impaired. TF transferrin, TFR1 transferrin receptor, ABCB7 ATP binding cassette subfamily B member 7, LPCAT3 lysophosphatidylcholine acyltransferase 3, ACC acetyl-CoA carboxylase, ALOX lipoxygenase, CISD1 CDGSH iron sulfur domain 1, CoQ coenzyme Q, Cys cysteine, Cys2 cystine, FTMT ferritin mitochondrial, GCL glutamate-cysteine ligase, GSH glutathione, GSSG oxidized glutathione, LIP labile iron pool, POR cytochrome P450 oxidoreductase, SLC25A37, solute carrier family 25 member37, SLC25A28 solute carrier family 25 member 28, ACSL-4, Acyl-CoA synthetase long-chain family member 4. This figure was created with BioRender.com