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(11,12) It is postulated that Thymosin beta-4 might exert this potential through its interactions with ATP synthase enzymes located on the cell surface, which are critical for cellular energy production

Overall, the resistance to ferroptosis of GPX4 requires catalytic selenocysteine residues and depletion of GSH, and inhibition of peroxide accumulation is achieved by GSR/GSH (glutathione disulfide reductase) and NADPH/H+ recirculation

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Declared that transmembrane member 16A (TMEM16A), a component of hepatocyte Ca 2+ -activated chloride channel, exacerbates hepatic I/R injury through the promotion of GPX4-dependent ferroptosis, and interrupting the TMEM16A-GPX4 interaction or inhibiting TMEM16A in liver cells may represent promising therapeutic strategies for the treatment of hepatic I/R injury [416]