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Cardiovasc Res. 2014 May 1;102(2):321-8. doi: 10.1093/cvr/cvu071. Epub 2014 Mar 27.

Macrophage migration inhibitory factor in myocardial ischaemia/reperfusion injury.

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Medical Faculty, Division of Cardiology, Pulmonology and Vascular Medicine, University Hospital Düsseldorf, Moorenstrasse 5, Düsseldorf D-40225, Germany.


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 protein-protein 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.


Cardioprotection; Macrophage migration inhibitory factor; Myocardial ischaemia/reperfusion injury

[Indexed for MEDLINE]

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