Journal
CARDIOVASCULAR RESEARCH
Volume 102, Issue 2, Pages 321-328Publisher
OXFORD UNIV PRESS
DOI: 10.1093/cvr/cvu071
Keywords
Macrophage migration inhibitory factor; Myocardial ischaemia; reperfusion injury; Cardioprotection
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Funding
- Deutsche Forschungsgemeinschaft (DFG) [Be1977/4-2, GRK1508/1]
- DFG [RA969/6-1, RA969/7-2]
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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.
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