Macrophage migration inhibitory factor in myocardial ischaemia/reperfusion injury

被引：72

作者：

Rassaf, Tienush ^{[1
]}

Weber, Christian ^{[2
]}

Bernhagen, Juergen ^{[3
]}

机构：

[1] Univ Hosp Dusseldorf, Med Fac, Div Cardiol Pulmonol & Vasc Med, D-40225 Dusseldorf, Germany

[2] Univ Munich, Inst Cardiovasc Prevent, Munich, Germany

[3] Rhein Westfal TH Aachen, Inst Biochem & Mol Cell Biol, Aachen, Germany

来源：

CARDIOVASCULAR RESEARCH | 2014年 / 102卷 / 02期

关键词：

Macrophage migration inhibitory factor; Myocardial ischaemia; reperfusion injury; Cardioprotection; ACTIVATED PROTEIN-KINASE; FACTOR MIF; SIGNALING PATHWAY; OXIDATIVE STRESS; CYTOKINE; ISCHEMIA; DYSFUNCTION; MECHANISMS; INFARCTION; DISEASE;

D O I：

10.1093/cvr/cvu071

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

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.

引用

页码：321 / 328

页数：8

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