Activation and Signaling by the AMP-Activated Protein Kinase in Endothelial Cells

The AMP-activated protein kinase (AMPK) was initially identified as the kinase that phosphorylates the 3-hydroxy 3-methylglutaryl coenzyme A reductase, the rate-limiting enzyme for cholesterol biosynthesis. As the name suggests, the AMPK is activated by increased intracellular concentrations of AMP,...

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Bibliographic Details
Published in:Circulation research 2009-07, Vol.105 (2), p.114-127
Main Authors: Fisslthaler, Beate, Fleming, Ingrid
Format: Article
Language:English
Subjects:
AMP-Activated Protein Kinases - antagonists & inhibitors
AMP-Activated Protein Kinases - metabolism
Animals
Atherosclerosis (general aspects, experimental research)
Biological and medical sciences
Blood and lymphatic vessels
Cardiology. Vascular system
Cardiovascular Diseases - drug therapy
Cardiovascular Diseases - enzymology
Endothelial Cells - drug effects
Endothelial Cells - enzymology
Energy Metabolism
Enzyme Activation
Enzyme Activators - pharmacology
Fundamental and applied biological sciences. Psychology
Gene Expression Regulation
Homeostasis
Humans
Isoenzymes
Medical sciences
NADPH Oxidases - metabolism
Nitric Oxide Synthase Type III - metabolism
Oxidation-Reduction
Phosphorylation
Protein Kinase Inhibitors - pharmacology
Proto-Oncogene Proteins c-akt - metabolism
Signal Transduction - drug effects
Vertebrates: cardiovascular system
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Summary:The AMP-activated protein kinase (AMPK) was initially identified as the kinase that phosphorylates the 3-hydroxy 3-methylglutaryl coenzyme A reductase, the rate-limiting enzyme for cholesterol biosynthesis. As the name suggests, the AMPK is activated by increased intracellular concentrations of AMP, and is generally described as a “metabolite-sensing kinase” and when activated initiates steps to conserve cellular energy. Although there is a strong link between the activity of the AMPK and metabolic control in muscle cells, the activity of the AMPK in endothelial cells can be regulated by stimuli that affect cellular ATP levels, such as hypoxia as well as by fluid shear stress, Ca-elevating agonists, and hormones such as adiponectin. To date the AMPK in endothelial cells has been implicated in the regulation of fatty acid oxidation, small G protein activity and nitric oxide production as well as inflammation and angiogenesis. Moreover, there is evidence indicating that the activation of the AMPK may help to prevent the vascular complications associated with the metabolic syndrome.
ISSN:0009-7330
1524-4571
DOI:10.1161/CIRCRESAHA.109.201590