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Description
The core argument is that estrogen acts as an endogenous, multi-target inhibitor of ferroptosis, conferring robust anti-ferroptotic capabilities to vascular cells by activating the Nrf2 central antioxidant system, optimizing cellular iron homeostasis (e.g., upregulating FPN1 and inhibiting ferritinophagy), and exerting direct antioxidant effects
One such study found that glutathione levels increased when vitamin D deficiency was corrected among children with nutritional rickets
, Zhang C., Wang J
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