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The basic mechanisms that regulate systemic iron have been elucidated, and these involve iron-dependent expression of liver hepcidin (Hep) and its interaction with ferroportin (Fpn) (excellent review on this topic in [5, 6]), while mechanisms that regulate brain iron are poorly known

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Unlike native IGF-1, which requires frequent administration due to its short half-life and extensive IGFBP binding, IGF-1 LR3's enhanced stability and bioavailability make it a more practical candidate for investigating growth factor-mediated tissue regeneration and metabolic regulation