The chemokine MCP-1 is thought to play a key role - among many other pathophysiological processes - in myocardial infarction. MCP-1 is not only a key attractant for monocytes and macrophages and as such responsible for inflammation but might also be directly involved in the modulation of repair processes in the heart. We show that cultured human cardiac cells express MCP-1 and that its expression is upregulated by inflammatory cytokines and downregulated by hypoxia. We hypothesize that inflammation but not hypoxia is the main trigger for monocyte recruitment in the human heart.