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Not for nothing is it widely considered the bodys master antioxidant

Deficiency of GPx1 also promotes pro-inflammatory activation of endothelial and other cell types, and accelerates atherogenesis in susceptible animal models [6, 78, 79, 84, 85]

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Regarding the integrated pathogenic network linking ferroptosis with inflammation, hypoxia, and fibrosis, in this network, the initial AKI-induced tubular injury (e.g., from I/R or nephrotoxicity) directly triggers ferroptosis via mitochondrial dysfunction and iron overload