Macrophage migration inhibitory factor in myocardial ischaemia/reperfusion injury

Acute myocardial infarction (AMI) remains one of the leading causes of death in the developed world. There is emerging evidence that the cytokine macrophage migration inhibitory factor (MIF) is a crucial player in AMI. Cardioprotection by MIF is likely to be a multifactorial phenomenon mediated by receptor-mediated signalling processes, intracellular proteinprotein interactions, and enzymatic redox regulation. Co-ordinating several pathways in the ischaemic heart, MIF contributes to receptor-mediated regulation of cardioprotective AMP-activated protein kinase signalling, inhibition of pro-apoptotic cascades, and the reduction of oxidative stress in the post-ischaemic heart. Moreover, the cardioprotective properties of MIF are modulated by S-nitros(yl)ation. These effects in the pathophysiology of myocardial ischaemia/reperfusion injury qualify MIF as a promising therapeutic target in the future. We here summarize the findings of experimental and clinical studies and emphasize the therapeutic potential of MIF in AMI.