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Excessive dysregulations involving the hepcidin-ferroportin axis, DMT1–transferrin transport, ferritin–NCOA4-mediated ferritinophagy, and regulatory pathways like Nrf2, IRP/IRE, and SIRT1 intensify oxidative stress, ferroptosis and neuroinflammation in neurodegenerative and acute CNS disorders

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GHK-Cu actúa a nivel tisular y de expresión génica, promoviendo la producción de colágeno, la curación de heridas y la reparación celular con resultados visibles enfocados en la piel