Imbalances of iron homeostasis account for some of the most common human diseases. Pathologies result from both, iron deficiency or overload and frequently affect the hepcidin/ferroportin regulatory system that balances systemic iron metabolism. The small hepatic peptide hormone hepcidin orchestrates systemic iron fluxes and controls plasma iron levels by binding to the iron exporter ferroportin on the surface of iron releasing cells, triggering its degradation and hence reducing iron transfer to transferrin. Hepcidin thus maintains transferrin saturation at physiological levels assuring adequate iron supplies to all cell types. My presentation will focus on mechanisms that control hepcidin and ferroportin expression as well as on pathologies that arise when this key regulatory circuitry underlying systemic iron homeostasis is disrupted.
No relevant conflicts of interest to declare.
Author notes
Asterisk with author names denotes non-ASH members.
