Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

Cellular iron is required for the utilization of oxygen in the cell. Iron in iron-sulfur and heme groups is required for electron transfer and oxygen activation in oxidative phosphorylation, while labile free iron is required for oxygen activation by dioxygenases, and as a catalyst for redox signaling. At the same time, this reactivity with oxygen underpins the production of cell-damaging free radicals in the presence of excess iron. Because the cardiac cell is a major site of oxygen flux, it requires tight control of intracellular iron levels. Until recently, such control was thought to be mediated predominantly by the action of iron regulatory proteins. However, new evidence reveals that cardiomyocyte hepcidin is indispensable for the control of intracellular iron levels, normal metabolism and heart function. This new evidence highlights the need for better understanding of the regulation of cardiomyocyte hepcidin in health and disease.

Original publication





Publication Date





189 - 200


Cardiomyocyte, Ferroportin, Heart, Heart failure, Hepcidin, Hypoxia, Inflammation, Iron, Myocardial infarction, Animals, Gene Expression Regulation, Hepcidins, Homeostasis, Humans, Iron, Myocytes, Cardiac