Cited by 740Cardiac Ischemia and ReperfusionMetabolism, Diabetes, and CancerCardiovascular Function and Risk Factors

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AMP-activated protein kinase mediates ischemic glucose uptake and prevents postischemic cardiac dysfunction, apoptosis, and injury

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Russell, Raymond R., Li, Ji, Coven, David L., Pypaert, Marc, Zechner, Christoph, Palmeri, Monica, Giordano, Frank J., Mu, James, Birnbaum, Morris J., Young, Lawrence H.·2004·Journal of Clinical Investigation

DOI 10.1172/jci19297PMC PMC503766

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Abstract

AMP-activated protein kinase (AMPK) is an important regulator of diverse cellular pathways in the setting of energetic stress.Whether AMPK plays a critical role in the metabolic and functional responses to myocardial ischemia and reperfusion remains uncertain.We examined the cardiac consequences of long-term inhibition of AMPK activity in transgenic mice expressing a kinase dead (KD) form of the enzyme.The KD mice had normal fractional shortening and no heart failure, cardiac hypertrophy, or fibrosis, although the in vivo left ventricular (LV) dP/dt was lower than that in WT hearts.During low-flow ischemia and postischemic reperfusion in vitro, KD hearts failed to augment glucose uptake and glycolysis, although glucose transporter content and insulin-stimulated glucose uptake were normal.KD hearts also failed to increase fatty acid oxidation during reperfusion.Furthermore, KD hearts demonstrated significantly impaired recovery of LV contractile function during postischemic reperfusion that was associated with a lower ATP content and increased injury compared with WT hearts.Caspase-3 activity and TUNEL-staining were increased in KD hearts after ischemia and reperfusion.Thus, AMPK is responsible for activation of glucose uptake and glycolysis during low-flow ischemia and plays an important protective role in limiting damage and apoptotic activity associated with ischemia and reperfusion in the heart.Nonstandard abbreviations used: acetyl-CoA carboxylase (ACC); 5-aminoimidazole-4-carboxamide-1-β-4-ribofuranoside (AICAR); AMP-activated protein kinase (AMPK); carnitine palmitoyltransferase-1 (CPT-1); kinase dead (KD); left ventricular (LV); LV developed pressure (LVDP); 6-phosphofructo-2-kinase (PFK-2). Conflict of interest:The authors have declared that no conflict of interest exists.

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Authors: Russell, R. R., Li, J., Coven, D. L., Pypaert, M., Zechner, C., Palmeri, M., Giordano, F. J., Mu, J., Birnbaum, M. J., & Young, L. H.
Affiliations: Yale University (US)
Howard Hughes Medical Institute (US)
Corresponding author: Young, Lawrence H.
ORCID: Li, Ji
Zechner, Christoph
Mu, James
Birnbaum, Morris J.
Young, Lawrence H.
Venue: Journal of Clinical Investigation
Publisher: American Society for Clinical Investigation
Published: 2004-08-16
Volume: 114
Issue: 4
Pages: 495-503
ISSN: 0021-9738 (ISSN-L)
DOI: 10.1172/jci19297
PMC: PMC503766
OpenAlex: W2073534977
Cited by: 738
References: 74
Citations by year: 2026: 10 · 2025: 16 · 2024: 16 · 2023: 19 · 2022: 28 · 2021: 30 · 2020: 23 · 2019: 26 · 2018: 28 · 2017: 31 · 2016: 40 · 2015: 36 · 2014: 42 · 2013: 34 · 2012: 52
FWCI: 24.26
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Journal of Clinical Investigation (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: Howard Hughes Medical Institute
American Heart Association
Yale University
Deutscher Akademischer Austauschdienst
Raymond and Beverly Sackler Institute for Biological, Physical and Engineering Sciences, Yale University
U.S. Public Health Service (U24 DK59635)
National Heart, Lung, and Blood Institute (R01HL063811, R01-HL-63811, HL 10301, F32HL010301)
National Institute of Diabetes and Digestive and Kidney Diseases (U24DK59635, U24DK059635)
Topics: Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Ischemia and Reperfusion
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
Keywords: AMPK, myocardial ischemia, ischemia-reperfusion injury, glucose uptake, glycolysis, cardiac contractile function, apoptosis, caspase-3, fatty acid oxidation, ATP levels, cardioprotection, energy metabolism
MeSH terms: Animals, Glucose, Glycolysis, Mice, Inbred C57BL, Mice, Transgenic, Multienzyme Complexes, Myocardial Reperfusion Injury, Myocardial Ischemia, Apoptosis, Protein Serine-Threonine Kinases, Mice, AMP-Activated Protein Kinases

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AMP-activated protein kinase mediates ischemic glucose uptake and prevents postischemic cardiac dysfunction, apoptosis, and injury

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