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Hydroxylation is the predominant metabolic pathway in early neonatal life, whereas glucuronidation increases as UGT1A9 activity matures postnatally (119, 202)

470 In animal models of Apelin-13-caused cardiomyocyte hypertrophy and heart failure, NCOA4-activated ferritinophagy leads to the upregulation of SFXN1 expression, causing mitochondrial iron overload and mitochondrial ROS overproduction, increased lipid peroxidation, and ultimately, ferroptosis

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These results imply a significant transfer of electrons from the hydroxide to the Ru atoms, leading to Ru sites with a high electron density for efficient ROS biocatalysis