First discovered in 1966 as an inflammatory cytokine, MIF (macrophage migration inhibitory factor) has been extensively studied for its pivotal role in a variety of inflammatory diseases, including rheumatoid arthritis and atherosclerosis. Although initial studies over a decade ago reported increases in circulating MIF levels following acute MI (myocardial infarction), the dynamic changes in MIF and its pathophysiological significance following MI have been unknown until recently. In the present review, we summarize recent experimental and clinical studies examining the diverse functions of MIF across the spectrum of acute MI from brief ischaemia to post-infarct healing. Following an acute ischaemic insult, MIF is rapidly released from jeopardized cardiomyocytes, followed by a persistent MIF production and release from activated immune cells, resulting in a sustained increase in circulating levels of MIF. Recent studies have documented two distinct actions of MIF following acute MI. In the supra-acute phase of ischaemia, MIF mediates cardioprotection via several distinct mechanisms, including metabolic activation, apoptosis suppression and antioxidative stress. In prolonged myocardial ischaemia, however, MIF promotes inflammatory responses with largely detrimental effects on cardiac function and remodelling. The pro-inflammatory properties of MIF are complex and involve MIF derived from cardiac and immune cells contributing sequentially to the innate immune response evoked by MI. Emerging evidence on the role of MIF in myocardial ischaemia and infarction highlights a significant potential for the clinical use of MIF agonists or antagonists and as a unique cardiac biomarker.
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Review Article|
April 03 2014
Role of MIF in myocardial ischaemia and infarction: insight from recent clinical and experimental findings
Nalin H. Dayawansa;
Nalin H. Dayawansa
1
*Experimental Cardiology Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, Australia
†Department of Cardiovascular Medicine, Alfred Hospital, Melbourne, Australia
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Xiao-Ming Gao;
Xiao-Ming Gao
1
*Experimental Cardiology Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, Australia
‡Department of Surgery, Central Clinical School, Monash University, Melbourne, Australia
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David A. White;
David A. White
*Experimental Cardiology Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, Australia
§Department of Medicine, Central Clinical School, Monash University, Melbourne, Australia
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Anthony M. Dart;
Anthony M. Dart
*Experimental Cardiology Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, Australia
†Department of Cardiovascular Medicine, Alfred Hospital, Melbourne, Australia
§Department of Medicine, Central Clinical School, Monash University, Melbourne, Australia
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Xiao-Jun Du
*Experimental Cardiology Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, Australia
†Department of Cardiovascular Medicine, Alfred Hospital, Melbourne, Australia
§Department of Medicine, Central Clinical School, Monash University, Melbourne, Australia
Correspondence: Dr Xiao-Jun Du (email [email protected]).
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Publisher: Portland Press Ltd
Received:
January 09 2014
Revision Received:
March 03 2014
Accepted:
March 11 2014
Online ISSN: 1470-8736
Print ISSN: 0143-5221
© The Authors Journal compilation © 2014 Biochemical Society
2014
Clin Sci (Lond) (2014) 127 (3): 149–161.
Article history
Received:
January 09 2014
Revision Received:
March 03 2014
Accepted:
March 11 2014
Citation
Nalin H. Dayawansa, Xiao-Ming Gao, David A. White, Anthony M. Dart, Xiao-Jun Du; Role of MIF in myocardial ischaemia and infarction: insight from recent clinical and experimental findings. Clin Sci (Lond) 1 August 2014; 127 (3): 149–161. doi: https://doi.org/10.1042/CS20130828
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