Fig. 3: Ferroptosis-associated TFs regulate the emerging hallmarks of neurological diseases. | Experimental & Molecular Medicine

Fig. 3: Ferroptosis-associated TFs regulate the emerging hallmarks of neurological diseases.

From: Ferroptosis-associated transcriptional factors in neurological diseases: molecular mechanisms and therapeutic prospects

Fig. 3

The figure shows how TFs affect ferroptosis in neurological diseases (for example, AD, PD, epilepsy and stroke) and their relationships with disease phenotypes. a In AD, TF-mediated regulation of ferroptosis is linked to disease phenotypes such as Aβ deposition, tau hyperphosphorylation, OS and neuroinflammation. b In PD, TF-mediated regulation of ferroptosis is involved in its disease phenotypes such as α-synuclein aggregation, OS and neuroinflammation. c In epilepsy, ferroptosis-related TFs can affect neuronal hyperexcitability, mitochondrial dysfunction, neuroinflammation and neurogenesis. d In stroke, ferroptosis-associated TFs regulate the formation of thrombus, OS and neuroinflammation. PUFA-CoA, polyunsaturated fatty acyl–coenzyme A; PUFA-PL, polyunsaturated fatty acid-containing phospholipids; PLOOH, phospholipid hydroperoxides; STEAP3, six-transmembrane epithelial antigen of prostate 3; FTL, ferritin light chain; FTH1, ferritin heavy chain 1; GSSG, oxidized GSH; R-OH, hydroxylated lipid; R-OOH, lipid hydroperoxide; SLC3A2, solute carrier family 3 member 2; PLA2G4, phospholipase A2 group IVA; ⟶, activation; ⊣, inhibition.

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