Vasohibin was recently isolated as an angiogenesis inhibitor, whose expression was augmented in endothelial cells by stimulation of vascular endothelial growth factor (VEGF) - the most crucial stimulator of angiogenesis, thus indicating its role as negative feedback regulator. Both animal studies and clinical trials have shown the potential positive benefit of VEGF for the revascularization after myocardial ischemia. The expression of vasohibin in the human heart, which could possibly influence the VEGF-mediated stimulation of angiogenesis, however, was so far unknown. Therefore we investigated the expression and regulation of vasohibin-1 in the human heart. We could show that vasohibin-1 was present in the human heart and that it was predominantly expressed in the nuclei and cytoplasms of cardiac cells. Furthermore, anoxia inhibited the vasohibin-1 expression in human adult cardiac myocytes. We therefore suggest that vasohibin-1 might interfere with current angiogenic therapies. The presence of the protein in the nucleus and the fact, that its mechanism of action is so far unknown, raises a lot of questions, that should be implicated in future studies.