Iron-mediated injury plays an important role in a number of heart disorders. Studies on heart iron are therefore crucial for understanding the causes of excessive heart iron. Heart cells have the ability to accumulate transferrin-bound-iron via the transferrin receptor and non-transferrin-bound-iron probably via the L-type Ca2+ channel and the divalent metal transporter1. However, little is known about the mechanisms of iron export in the heart cells. Here, we investigated expression of iron exporters including ferroportin 1 (Fpn1), ceruloplasmin (CP) and hephaestin (Heph) and provided evidence for their existence in the heart. We demonstrated that iron has a significant effect on expression of Fpn1 and CP, but not Heph. Treatment of a high-iron diet induced a significant increase in Fpn1, a decrease in CP but no change in Heph mRNA and protein. The control of Fpn1 and CP protein expression by iron was parallel to that of their mRNA expression, suggesting a transcriptional regulation of Fpn1 and CP by iron. The existence of these proteins in the heart implies that they might have a role in heart iron homeostasis.