| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 9186369 | Trends in Cardiovascular Medicine | 2005 | 9 Pages |
Abstract
AMP-activated protein kinase (AMPK) is activated during exercise and ischemia and is emerging as an important regulatory mechanism in the heart. AMPK promotes adenosine triphosphate-generating pathways, including glucose transport, glycolysis, and fatty acid oxidation, while inhibiting energy-consuming anabolic pathways. After ischemia-reperfusion, AMPK-deficient hearts from transgenic mice have severe left ventricular contractile dysfunction with increased apoptosis and necrosis. Mutations in the AMPKγ2 subunit lead to cardiac glycogen overload, Wolff-Parkinson-White syndrome, arrhythmias, and heart failure. This review focuses on the molecular mechanisms of activation and cardiovascular actions of AMPK in the heart.
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Authors
Lawrence H. Young, Ji Li, Suzanne J. Baron, Raymond R. Russell,