Preclinical and clinical assessment of the beneficial effects of hepcidin, a pivotal endogenous regulator of iron metabolism, on anthracycline-induced cardiotoxicity.

Mitochondrial iron overload in cardiac myocytes is associated with anthracycline-induced cardiotoxicity due to excess reactive oxygen species generation. Cancer can induce an inflammatory state, characterized by the inability of the organism to deliver stored iron to metabolizing tissues due to high circulating hepcidin levels (‘hepcidin block’). We are investigating the beneficial role of hepcidin on anthracycline-induced cardiotoxicity, both in a murine model as well as in a clinical study.