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Trends Endocrinol Metab. 2015 Aug;26(8):422-9. doi: 10.1016/j.tem.2015.05.010. Epub 2015 Jul 6.

AMPK: energy sensor and survival mechanism in the ischemic heart.

Author information

1
The Sections of Cardiovascular Medicine, Yale University School of Medicine, 333 Cedar Street, 3 FMP, P.O. Box 208017, New Haven, CT 06520-8017, USA.
2
The Sections of Cardiovascular Medicine, Yale University School of Medicine, 333 Cedar Street, 3 FMP, P.O. Box 208017, New Haven, CT 06520-8017, USA; Department of Internal Medicine, Yale University School of Medicine, 333 Cedar Street, 3 FMP, P.O. Box 208017, New Haven, CT 06520-8017, USA; Department of Cellular and Molecular Physiology, Yale University School of Medicine, 333 Cedar Street, 3 FMP, P.O. Box 208017, New Haven, CT 06520-8017, USA. Electronic address: Lawrence.young@yale.edu.

Abstract

AMP-activated protein kinase (AMPK) is a critical regulator of cellular metabolism and plays an important role in diabetes, cancer, and vascular disease. In the heart, AMPK activation is an essential component of the adaptive response to cardiomyocyte stress that occurs during myocardial ischemia. During ischemia-reperfusion, AMPK activation modulates glucose and fatty acid metabolism, mitochondrial function, endoplasmic reticulum (ER) stress, autophagy, and apoptosis. Pharmacological activation of AMPK prevents myocardial necrosis and contractile dysfunction during ischemia-reperfusion and potentially represents a cardioprotective strategy for the treatment of myocardial infarction. This review discusses novel mechanisms of AMPK activation in the ischemic heart, the role of endogenous AMPK activation during ischemia, and the potential therapeutic applications for AMPK-directed therapy.

PMID:
26160707
PMCID:
PMC4697457
DOI:
10.1016/j.tem.2015.05.010
[Indexed for MEDLINE]
Free PMC Article

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