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In the case of eNOS uncoupling due to relative intracellular BH 4 deficiency, this phenomenon could be prevented by simultaneous overexpression of the BH 4 synthesizing enzyme GTP cyclohydrolase I, which has been demonstrated in isolated cells 92 and in atherosclerotic animal models

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Although TFRCs involvement in ferroptosis is consistent with prior studies, its regulation by ascites and potential contribution to peritoneal metastasis represent previously uncharacterized aspects of this pathway