Testosterone Perturbs Systemic Iron Balance Through Activation of Epidermal Growth Factor Receptor Signaling in the Liver and Repression of Hepcidin

Abstract

Testosterone-induced repression of hepcidin expression becomes functionally important during homeostatic stress from disorders that result in iron loading and/or reduced capacity for hepcidin synthesis. These findings suggest that novel therapeutic strategies targeting the testosterone/EGF/EGFR axis may be useful for inducing hepcidin expression in patients with iron overload and/or chronic liver diseases.