We are analyzing https://link.springer.com/article/10.1007/s12185-012-1069-y.

Title:
Hypoxia-inducible factors and their roles in energy metabolism | International Journal of Hematology
Description:
Over the course of evolution, aerobic organisms have developed sophisticated systems for responding to alterations in oxygen concentration, as oxygen acts as a final electron acceptor in oxidative phosphorylation for energy production. Hypoxia-inducible factor (HIF) plays a central role in the adaptive regulation of energy metabolism, by triggering a switch from mitochondrial oxidative phosphorylation to anaerobic glycolysis in hypoxic conditions. HIF also reduces oxygen consumption in mitochondria by inhibiting conversion of pyruvate to acetyl CoA, suppressing mitochondrial biogenesis and activating autophagy of mitochondria concomitantly with reduction in reactive oxygen species production. In addition, metabolic reprogramming in response to hypoxia through HIF activation is not limited to the regulation of carbohydrate metabolism; it occurs in lipid metabolism as well. Recent studies using in vivo gene-targeting technique have revealed unexpected, but novel functions of HIF in energy metabolism in a context- and cell type-specific manner, and shed light on the possibility of pharmaceutical targeting HIF as a new therapy against many diseases, including cancer, diabetes, and fatty liver.
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Keywords {🔍}

hif, article, oxygen, liver, google, scholar, pubmed, cas, metabolism, hypoxia, cell, mitochondrial, factor, lipid, expression, cells, hypoxiainducible, energy, metabolic, mice, hypoxic, fatty, activation, regulation, glycolysis, consumption, induction, glucose, hifα, production, mitochondria, gene, pyruvate, response, activity, conditions, hifs, data, cancer, hifmediated, roles, ros, kinase, reduction, addition, dehydrogenase, cmyc, hepatic, accumulation, acid,

Topics {✒️}

hif-1α-deficient mefs fails hif-1α-deficient mice fed hypoxia-inducible factor-1-mediated expression counteracts c-myc activity high-fat/sucrose diets [36] hif1alpha-ppargamma axis underlies hif-1α-deficient mice c-myc-max interaction phd2/3 double-knockout mice hif-2α-deficient mice hypoxia-inducible factor signalling affects hif-1-mediated regulations v-src induces expression lipid anabolic pathways hif-related gene results diet-induced obese mice diet-induced obesity mice hif-mediated metabolic alterations cell type-specific manner c-myc binding c-myc activity hypoxia-induced mitochondrial fission fatty acid synthesis iron–sulfur cluster [22] iron–sulfur cluster de novo lipogenesis c-myc antagonist specific target gene hypoxia-elicited pdh inhibition vivo gene-targeting technique directly reducing oxygen vhl-deficient liver [38] severe lipid accumulation hif-1-mediated dec1 activation renal cell carcinoma privacy choices/manage cookies critical transcription factor oxygen-independent atp production hypoxia-inducible factors promote metabolic reprogramming hif-1-mediated pdk1 induction hypoxia-inducible factor hypoxia-inducible factor-1 hypoxia-inducible factor 1 hypoxia inducible factor kim jw lipid droplet protein related gene expressions antagonizing myc function inhibits mitochondrial biogenesis

Schema {🗺️}

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         description:Over the course of evolution, aerobic organisms have developed sophisticated systems for responding to alterations in oxygen concentration, as oxygen acts as a final electron acceptor in oxidative phosphorylation for energy production. Hypoxia-inducible factor (HIF) plays a central role in the adaptive regulation of energy metabolism, by triggering a switch from mitochondrial oxidative phosphorylation to anaerobic glycolysis in hypoxic conditions. HIF also reduces oxygen consumption in mitochondria by inhibiting conversion of pyruvate to acetyl CoA, suppressing mitochondrial biogenesis and activating autophagy of mitochondria concomitantly with reduction in reactive oxygen species production. In addition, metabolic reprogramming in response to hypoxia through HIF activation is not limited to the regulation of carbohydrate metabolism; it occurs in lipid metabolism as well. Recent studies using in vivo gene-targeting technique have revealed unexpected, but novel functions of HIF in energy metabolism in a context- and cell type-specific manner, and shed light on the possibility of pharmaceutical targeting HIF as a new therapy against many diseases, including cancer, diabetes, and fatty liver.
         datePublished:2012-04-26T00:00:00Z
         dateModified:2012-04-26T00:00:00Z
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            Hematology
            Oncology
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      headline:Hypoxia-inducible factors and their roles in energy metabolism
      description:Over the course of evolution, aerobic organisms have developed sophisticated systems for responding to alterations in oxygen concentration, as oxygen acts as a final electron acceptor in oxidative phosphorylation for energy production. Hypoxia-inducible factor (HIF) plays a central role in the adaptive regulation of energy metabolism, by triggering a switch from mitochondrial oxidative phosphorylation to anaerobic glycolysis in hypoxic conditions. HIF also reduces oxygen consumption in mitochondria by inhibiting conversion of pyruvate to acetyl CoA, suppressing mitochondrial biogenesis and activating autophagy of mitochondria concomitantly with reduction in reactive oxygen species production. In addition, metabolic reprogramming in response to hypoxia through HIF activation is not limited to the regulation of carbohydrate metabolism; it occurs in lipid metabolism as well. Recent studies using in vivo gene-targeting technique have revealed unexpected, but novel functions of HIF in energy metabolism in a context- and cell type-specific manner, and shed light on the possibility of pharmaceutical targeting HIF as a new therapy against many diseases, including cancer, diabetes, and fatty liver.
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      dateModified:2012-04-26T00:00:00Z
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         Mitochondria
         Lipid metabolism
         HIF
         Hematology
         Oncology
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