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The present review is aimed at providing a synopsis of the involvement of MIF in the inflammatory pathogenesis of atherosclerosis and its consequences, namely unstable plaque formation, remodeling after arterial injury, aneurysm formation, myocardial infarction, or ischemia-reperfusion injury. In addition, other forms of myocardial dysfunction and inflammation and the role of MIF in angiogenesis are reviewed. The functional data are reconciled with recent progress in the identification of heptahelical (CXC chemokine) receptors for MIF, its prototypic role as their noncanonical ligand, and its signal transduction profile operative in atherogenic and inflammatory recruitment of mononuclear cells and in the oxidative damage and apoptosis of cardiomyocytes. Its unique features and functions clearly distinguish MIF from other cytokines implicated in atherogenesis and make it a prime target for achieving therapeutic regression of atherosclerosis. The potential of targeting or exploiting MIF for therapeutic strategies or as a diagnostic marker in the management of cardiovascular diseases or disorders is scrutinized.<\/jats:p>","DOI":"10.1161\/circulationaha.107.729125","type":"journal-article","created":{"date-parts":[[2008,3,24]],"date-time":"2008-03-24T16:44:35Z","timestamp":1206377075000},"page":"1594-1602","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":243,"title":["Macrophage Migration Inhibitory Factor in Cardiovascular Disease"],"prefix":"10.1161","volume":"117","author":[{"given":"Alma","family":"Zernecke","sequence":"first","affiliation":[{"name":"From the Institute for Molecular Cardiovascular Research (A.Z., C.W.) and Department of Biochemistry and Molecular Cell Biology (J.B.), Molekulare Herz-Kreislaufforschung, RWTH Aachen University, Aachen, 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