AMP‐activated protein kinase – development of the energy sensor concept

By D. Hardie, S. Hawley, J. Scott. Journal of Physiology, 2006

854 citations recorded by the source corpus.

Subfields: Molecular Biology, Physiology, Surgery

View Paper: https://www.semanticscholar.org/paper/360e77074b436138223e652340e8f9da5cc4531e

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In Molecular Biology

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Citations in the corpus

• AMP-activated protein kinase promotes macrophage polarization to an anti-inflammatory functional phenotype (2008, neutral): “In liver, active AMPK inhibits fatty acid synthesis and cholesterol synthesis (7) while in heart and skeletal muscle it stimulates fatty acid oxidation and glycolysis (8,9).”
• Glucose restriction inhibits skeletal myoblast differentiation by activating SIRT1 through AMPK-mediated regulation of Nampt. (2008, background): “In response to ATP depletion, the AMP-activated protein kinase (AMPK) is phosphorylated and activated (Hardie et al., 2006).”
• Butyrate enhances the intestinal barrier by facilitating tight junction assembly via activation of AMP-activated protein kinase in Caco-2 cell monolayers. (2009, background): “AMPK functions as a cellular fuel gauge that regulates metabolic pathways in glucose and fatty acid metabolism and protein synthesis (19).”
• Membrane fatty acid transporters as regulators of lipid metabolism: implications for metabolic disease. (2010, background): “Under conditions that favor a rapid increase in intracellular AMP, such as during increased contractile activity in muscle (477) or during a period of cardiac ischemia (259), AMPK becomes activated, resulting in the activation of catabolic pathways, such as the increased oxidation of fatty acids (ex”
• Cutting Edge: Distinct Glycolytic and Lipid Oxidative Metabolic Programs Are Essential for Effector and Regulatory CD4+ T Cell Subsets (2011, background): “In contrast, the AMPK pathway acts to inhibit mTOR by suppressing mTOR signaling and to promote mitochondrial oxidative metabolism rather than glycolysis (10).”
• Mechanisms of Vascular Aging (2018, background): “AMPK signaling is an important energy-sensing pathway that is involved in regulation of aging processes, integrating energy balance, metabolism, and cellular stress resistance.(185,186) In lower organisms, increased AMPK activity was shown to extend life span.”
• Extending life span by increasing oxidative stress. (2011, neutral): “additional health-promoting implications [57].”
• How increased oxidative stress promotes longevity and metabolic health: The concept of mitochondrial hormesis (mitohormesis). (2010, background): “…established as a sensor of cellular energy depletion in both mammals (Hardie et al., 2006) and specifically C. elegans (Apfeld et al., 2004; Greer et al., 2007), and has been found to induce a health-promoting metabolic state particularly by inducing mitochondrial metabolism (Hardie et al., 2006).”