Macrophage migration inhibitory factor stimulates AMP-activated protein kinase in the ischaemic heart

Edward J. Miller, Ji Li, Lin Leng, Courtney McDonald, Toshiya Atsumi, Richard Bucala and Lawrence H. Young ()
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Edward J. Miller: Cardiovascular Medicine Section of the Department of Internal Medicine,
Ji Li: Cardiovascular Medicine Section of the Department of Internal Medicine,
Lin Leng: Rheumatology Section of the Department of Internal Medicine,
Courtney McDonald: Rheumatology Section of the Department of Internal Medicine,
Toshiya Atsumi: Hokkaido University, Sapporo, 060-8638, Japan
Richard Bucala: Rheumatology Section of the Department of Internal Medicine,
Lawrence H. Young: Cardiovascular Medicine Section of the Department of Internal Medicine,

Nature, 2008, vol. 451, issue 7178, 578-582

Abstract: The heart under stress AMPK (AMP-activated protein kinase) is a master regulator of many biological processes and is a potential drug target for diseases as diverse as diabetes, cancer, atherosclerosis and ischaemic heart disease. In the ischaemic heart, AMPK protects tissues from injury and apoptosis by promoting glucose uptake. A new study shows that AMPK is activated by the inflammatory cytokine MIF (macrophage migration inhibitory factor), which is released by the heart under ischaemic stress. This throws new light on the nature of the cellular stress response, and highlights low MIF levels as a potential risk marker for patients with coronary artery disease.

Date: 2008
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DOI: 10.1038/nature06504

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