Crosstalk between Oxidative Stress and Ferroptosis/Oxytosis in Ischemic Stroke: Possible Targets and Molecular Mechanisms

Figure 1

Possible targets and molecular mechanisms of the crosstalk between oxidative stress and ferroptosis/oxytosis in ischemic stroke. Red boxes and spikes indicate potential mechanisms after ischemic stroke, with upward spikes indicating an increase and downward spikes indicating a decrease. Abbreviations: AA: arachidonic acid; AdA: adrenic acid; ACSL4: acyl-CoA synthetase long-chain family member 4; ARE: antioxidant response element; CP: ceruloplasmin; GCL: glutamate cysteine ligase; Glu: glutamate; GSS: glutathione synthetase; GSSG: oxidized GSH; HIF-PHD 1: hypoxia-inducible factor prolyl-hydroxylase 1; H₂O₂: hydrogen peroxide; 4-HNE: 4-hydroxynonenal; LPCAT3: lysophosphatidylcholine acyltransferase 3; MAF: muscle tendon fibrosarcoma protein; MDA: malondialdehyde; OH·: hydroxyl radical; sGC: soluble guanylate cyclase; STEAP3: six-transmembrane epithelial antigen of the prostate 3.