Systemic iron deficiency concomitant with macrophage iron retention is characteristic of iron-refractory anaemias associated
with chronic disease. The systemic misdistribution of iron, which is further exacerbated by parenteral iron supplementation,
is mainly attributable to iron retention exerted on resident macrophages by hepcidin-mediated down-regulation of the
iron exporter ferroportin. We aimed at developing an experimental macrophage-based cell model that recapitulates
pathophysiological features of iron misdistribution found in chronic disorders and use it as a screening platform for identifying
agents with the potential for relocating the accumulated metal and restoring affected functions.