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GSH production is supported by NRF2 through controlling several enzymes responsible for GSH synthesis, such as the glutamate-cysteine ligase (GCL) complex composed of two subunits, the modifier (GCLM) subunit and the catalytic (GCLC) subunit, which catalyze the rate-limiting step of GSH synthesis that converts cysteine and glutamate into GSH [22]

By remaining active for several days, it produces a more continuous elevation in growth hormone and insulin-like growth factor-1 (IGF-1)

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Under ischemic conditions, ferroptosis in transplanted endothelial cells enhances neutrophil recruitment to damaged cardiac tissue through upregulation of adhesion molecules and chemokine gradients [168]

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