Figure 7
From: Ferroptosis is involved in focal segmental glomerulosclerosis in rats
Ferroptosis involved in FSGS in Rats. Fe3+ is transported to cells via TF and TFR. Subsequently, Fe3+ is reduced to Fe2+ and released into LIP. NCOA4 binds to FTH1 and mediate ferritinophagy, increasing the accessibility of Fe2+ and inducing ferroptosis. Meanwhile, as a key antioxidant pathway, the system Xc−- GSH-GPX4 axis is damaged and promote lipid peroxidation and ferroptosis. PUFAs is converted to PUFA-PL via ACSL4 and generate PL-PUFA-OOH, thus driving ferroptosis. (Abbreviations: FSGS, focal segmental glomerulosclerosis; GSH, glutathione; GPX4, glutathione peroxidase 4; PUFAs, polyunsaturated fatty acids; ACSL4, acyl-CoA synthase long-chain family member 4; PUFA-PL, polyunsaturated fatty acids of phospholipids; MDA, Malondialdehyde; Fe2+, ferrous iron; PL-PUFA-OOH, phospholipid hydroperoxides; Fe3+, ferric iron; TF, transferrin; TFRC, transferrin receptor; LIP, labile iron pool; FTH1, ferritin heavy chain 1; FTL, ferritin light chain; NCOA4, nuclear receptor coactivator 4).
