Activation and Signaling by the AMP-Activated Protein Kinase in Endothelial Cells
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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(2+)-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.
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An increase in the activity of AMPK would also explain the protective effects of metformin on endothelial function via the activation of endothelial nitric oxide synthase, thereby countering the negative effects of a diabetic milieu on cardiovascular function.
“An increase in the activity of AMPK would also explain the protective effects of metformin on endothelial function via the activation of endothelial nitric oxide synthase (eNOS) thereby countering the negative effects of a diabetic milieu on cardiovascular function (119).”
From A Critical Review of the Evidence That Metformin Is a Putative Anti-Aging Drug That Enhances Healthspan and Extends Lifespan (2021) · cites this paper as [119]
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- Authors
- Fisslthaler, B., & Fleming, I.
- Affiliations
- Goethe University Frankfurt (DE)
- Venue
- Circulation Research
- Published
- 2009-07-17
- Volume
- 105
- Issue
- 2
- Pages
- 114-127
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- OpenAlex
- W2117748926
- Cited by
- 295
- References
- 165
- Citations by year
- 2026: 4 · 2025: 7 · 2024: 6 · 2023: 7 · 2022: 10 · 2021: 17 · 2020: 15 · 2019: 14 · 2018: 18 · 2017: 14 · 2016: 22 · 2015: 27 · 2014: 20 · 2013: 22 · 2012: 29
- FWCI
- 2.29
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Circulation Research (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Keywords
- AMPK, endothelial cells, AMPK signaling, energy sensing, hypoxia, fluid shear stress, adiponectin, fatty acid oxidation, small GTPases, nitric oxide production, inflammation, angiogenesis, metabolic syndrome, vascular complications
- MeSH terms
- Animals, Cardiovascular Diseases, Energy Metabolism, Enzyme Activation, Gene Expression Regulation, Homeostasis, Humans, Isoenzymes, Oxidation-Reduction, Phosphorylation, Signal Transduction, NADPH Oxidases, Enzyme Activators, Endothelial Cells, Protein Kinase Inhibitors, Proto-Oncogene Proteins c-akt, Nitric Oxide Synthase Type III, AMP-Activated Protein Kinases
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