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Journal of Biological Chemistry, ISSN 0021-9258, 07/2012, Volume 287, Issue 31, pp. 25758 - 25769
The early initiation phase of acute inflammation is anabolic and primarily requires glycolysis with reduced mitochondrial glucose oxidation for energy, whereas... 
MACROPHAGE-MEDIATED INFLAMMATION | HOMEOSTASIS | T-CELL MEMORY | METABOLISM | ADIPONECTIN | INSULIN-RESISTANCE | IMMUNOSUPPRESSION | BIOCHEMISTRY & MOLECULAR BIOLOGY | ENDOTOXIN TOLERANCE | SEPSIS | DIFFERENTIATION | Sirtuin 1 - metabolism | Humans | Monocyte-Macrophage Precursor Cells - immunology | Glucose Transporter Type 1 - metabolism | Monocyte-Macrophage Precursor Cells - metabolism | Leukocytes - immunology | Heat-Shock Proteins - genetics | Monocyte-Macrophage Precursor Cells - physiology | Nicotinamide Phosphoribosyltransferase - metabolism | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Sepsis - metabolism | Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha | NAD - biosynthesis | Fatty Acids - metabolism | Cell Line | Sepsis - immunology | Cytokines - metabolism | Oxidation-Reduction | Hypoxia-Inducible Factor 1, alpha Subunit - genetics | Heat-Shock Proteins - metabolism | Mice, Inbred C57BL | Transcription Factors - genetics | Toll-Like Receptor 4 - metabolism | Transcription Factors - metabolism | Carrier Proteins - genetics | Adaptation, Physiological - immunology | Animals | Carrier Proteins - metabolism | Energy Metabolism | Lipopolysaccharides - pharmacology | Glucose - metabolism | Glycolysis | Mice | Leukocytes - metabolism | Sirtuins - metabolism | NAD | Sirtuins | Immunology | Acute Inflammation | Bioenergetics | PGC-1 | Sepsis | HIF-1α | Biosensors | Macrophages | Metabolism
Journal Article
Nature immunology, ISSN 1529-2908, 2016, Volume 17, Issue 4, pp. 406 - 413
The acute phase of sepsis is characterized by a strong inflammatory reaction. At later stages in some patients, immunoparalysis may be encountered, which is... 
SYSTEMIC INFLAMMATION | MESSENGER-RNA TRANSLATION | ACTIVATION | INTERFERON-GAMMA | IFN-GAMMA | MACROPHAGES | SIRTUIN 1 | DYSFUNCTION | IMMUNOLOGY | EXPRESSION | CELLULAR-METABOLISM | Prospective Studies | Humans | Middle Aged | Transcriptome | Immunoblotting | Male | Monocytes - metabolism | Monocytes - immunology | Lipopolysaccharides - immunology | Antifungal Agents - therapeutic use | Leukocytes - immunology | Young Adult | Sepsis - drug therapy | Immune Tolerance - immunology | Sepsis - metabolism | Adenosine Triphosphate - metabolism | Candidiasis, Invasive - drug therapy | Endotoxemia - immunology | Adult | Aspergillosis - metabolism | Female | Macrophages - immunology | NAD - metabolism | Aspergillosis - drug therapy | Cytokines - immunology | Sepsis - immunology | Interferon-gamma - therapeutic use | Lactic Acid - metabolism | Oxidative Phosphorylation | Oxygen Consumption | Energy Metabolism - immunology | Escherichia coli Infections - metabolism | Candidiasis, Invasive - metabolism | Immunity, Innate - immunology | Macrophages - metabolism | Animals | Candidiasis, Invasive - immunology | Glycolysis | Escherichia coli Infections - immunology | Mice | Endotoxemia - metabolism | Leukocytes - metabolism | Aspergillosis - immunology | Complications and side effects | Energy metabolism | Immune response | Bioenergetics | Abnormalities | Sepsis | Regulation | Leukocytes | Properties | Health aspects
Journal Article
Antioxidants & Redox Signaling, ISSN 1523-0864, 12/2011, Volume 15, Issue 11, pp. 2837 - 2854
Hepatic energy depletion has been described in severe sepsis, and lipopolysaccharide (LPS) has been shown to cause mitochondrial DNA (mtDNA) damage. To clarify... 
Original Research Communications | OXIDATIVE STRESS | LIVER-INJURY | PEROXYNITRITE | MANGANESE SUPEROXIDE-DISMUTASE | NITRIC-OXIDE SYNTHASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | ENDOCRINOLOGY & METABOLISM | ETHANOL | MICE | TRANSCRIPTION-FACTOR | RESPIRATORY FACTOR-I | EXPRESSION | Aconitate Hydratase - metabolism | Electron Transport Complex III - metabolism | Superoxide Dismutase - genetics | Reactive Oxygen Species - metabolism | Humans | Tumor Necrosis Factor-alpha - blood | Alanine Transaminase - blood | Electron Transport Complex I - metabolism | Tyrosine - analogs & derivatives | Electron Transport Complex IV - metabolism | DNA-Binding Proteins - metabolism | Nitric Oxide Synthase Type II - antagonists & inhibitors | Sepsis - metabolism | Adenosine Triphosphate - metabolism | ATP Synthetase Complexes - metabolism | Nitrites - blood | Transcription, Genetic | Superoxide Dismutase - metabolism | Iron - blood | Nitrates - blood | DNA, Mitochondrial - metabolism | High Mobility Group Proteins - metabolism | Liver - metabolism | Mice, Inbred C57BL | Mice, Transgenic | Thiobarbituric Acid Reactive Substances - metabolism | Iron - metabolism | Toll-Like Receptor 4 - metabolism | Hep G2 Cells | Transcription Factors - metabolism | Tyrosine - metabolism | Animals | Interferon-beta - pharmacology | Nitric Oxide Synthase Type II - genetics | Lipopolysaccharides - pharmacology | Interferon-beta - blood | Mice | Nitric Oxide Synthase Type II - metabolism | DNA damage | Physiological aspects | Septic shock | Mitochondrial DNA | Genetic aspects | Research | Health aspects | Risk factors | Lipopolysaccharides
Journal Article
Circulation Research, ISSN 0009-7330, 01/2016, Volume 118, Issue 2, pp. 241 - 253
RATIONALE:Fatty acid oxidation is transcriptionally regulated by peroxisome proliferator–activated receptor (PPAR)α and under normal conditions accounts for... 
heart failure | PPAR alpha | fatty acids | cardiac myocyte | heart | CARDIAC & CARDIOVASCULAR SYSTEMS | LIPID-METABOLISM | CONTRACTILE DYSFUNCTION | FATTY-ACID-METABOLISM | SUBSTRATE METABOLISM | MOUSE MODELS | ACTIVATED-RECEPTOR-ALPHA | FAILING HEART | INSULIN-RESISTANCE | PERIPHERAL VASCULAR DISEASE | ENERGY-METABOLISM | HEMATOLOGY | TRANSCRIPTIONAL REGULATION | Up-Regulation | Transcriptional Activation | Diabetes Mellitus, Experimental - genetics | Transfection | Time Factors | Kruppel-Like Transcription Factors - metabolism | Sepsis - metabolism | Transcription, Genetic | Diabetes Mellitus, Experimental - metabolism | Kruppel-Like Transcription Factors - deficiency | Binding Sites | Fatty Acids - metabolism | Diabetes Mellitus, Experimental - physiopathology | Sodium-Glucose Transporter 2 - genetics | Binding, Competitive | Cardiomyopathy, Dilated - genetics | Cell Line | Promoter Regions, Genetic | Oxidation-Reduction | Signal Transduction | Sodium-Glucose Transporter 2 - metabolism | Mice, Inbred C57BL | Genotype | PPAR alpha - genetics | Sepsis - physiopathology | Cardiomyopathy, Dilated - metabolism | Sepsis - genetics | Sodium-Glucose Transporter 2 - antagonists & inhibitors | Mice, Knockout | Triglycerides - metabolism | Phenotype | Animals | Cardiomyopathy, Dilated - physiopathology | Energy Metabolism | Proto-Oncogene Proteins c-jun - metabolism | Myocytes, Cardiac - metabolism | Protein Binding | PPAR alpha - metabolism | Kruppel-Like Transcription Factors - genetics | diabetic cardiacmyopathy | KLF5 | PPARα
Journal Article
Immunity, ISSN 1074-7613, 12/2012, Volume 37, Issue 6, pp. 1009 - 1023
Cytopenias are key prognostic indicators of life-threatening infection, contributing to immunosuppression and mortality. Here we define a role for... 
NALP1 | LETHAL TOXIN | IN-VIVO | DISEASE | BINDING-PROTEIN | DEATH | INFECTION | IMMUNOLOGY | TIR DOMAIN | LYMPHOCYTIC CHORIOMENINGITIS VIRUS | CASPASE-1 ACTIVATION | Inflammasomes - metabolism | Cytoskeletal Proteins - genetics | Dermatitis - immunology | Pancytopenia - immunology | Caspase 1 - metabolism | Interferon-gamma - metabolism | Hematopoiesis - drug effects | Inflammation - metabolism | T-Lymphocytes - metabolism | Interleukin-1beta - metabolism | Apoptosis Regulatory Proteins - genetics | Cytoskeletal Proteins - metabolism | Hematopoietic Stem Cells - virology | Hematopoietic Stem Cells - drug effects | Hematopoietic Stem Cells - metabolism | Inflammation - immunology | Apoptosis Regulatory Proteins - metabolism | Mice, Knockout | Pancytopenia - metabolism | Hematopoiesis - immunology | Animals | CARD Signaling Adaptor Proteins | Adaptor Proteins, Signal Transducing - genetics | Inflammation - genetics | T-Lymphocytes - immunology | Fluorouracil - pharmacology | Mice | Mutation | Adaptor Proteins, Signal Transducing - metabolism | Interleukin-18 - metabolism | Apoptosis | Dermatitis - metabolism | Chemotherapy | Research | Health aspects | Oncology, Experimental | Immunotherapy | Cancer | Proteins | Medical research | Disease | Councils | Bone marrow | Infections | Grants | Kinases | pyroptosis | inflammasome | IL-18 | progenitor cells | NLRP1 | cytopenia | IL-1β | sepsis
Journal Article
Autophagy, ISSN 1554-8627, 08/2016, Volume 12, Issue 8, pp. 1272 - 1291
Journal Article
Scientific Reports, ISSN 2045-2322, 03/2016, Volume 6, Issue 1, p. 23240
Sepsis is the principal cause of fatality in the intensive care units worldwide. It involves uncontrolled inflammatory response resulting in multi-organ... 
CELLS | SHOCK | ACTIVATION | RECOGNITION | PHOSPHORYLATION | MULTIDISCIPLINARY SCIENCES | IL-10 PRODUCTION | PROINFLAMMATORY CYTOKINES | INTERVENTION | SESQUITERPENE LACTONES | SEVERE SEPSIS | Tumor Necrosis Factor-alpha - metabolism | Sepsis - etiology | Sepsis - prevention & control | Apoptosis - drug effects | Monocytes - cytology | Humans | Monocytes - metabolism | NF-kappa B - metabolism | Phosphatidylinositol 3-Kinases - metabolism | Interleukin-1beta - metabolism | Interleukin-10 - metabolism | Female | Chemokine CCL2 - metabolism | Proto-Oncogene Proteins c-akt - metabolism | Interleukin-6 - metabolism | Cell Line | Sesquiterpenes, Guaiane - pharmacology | Lung - pathology | Lipopolysaccharides - toxicity | Anti-Inflammatory Agents - pharmacology | Liver - metabolism | Mice, Inbred C57BL | Macrophages - cytology | Toll-Like Receptor 4 - metabolism | Monocytes - drug effects | Macrophages - metabolism | Animals | Signal Transduction - drug effects | Macrophages - drug effects | RAW 264.7 Cells | Cell Proliferation - drug effects | Mice | Mitogen-Activated Protein Kinases - metabolism | Liver | AKT protein | Arthritis | Kinases | Macrophages | Immunosuppressive agents | Lipopolysaccharides | Interleukin 6 | Intensive care units | Cell activation | Intestine | Rodents | Gram-negative bacteria | Peritonitis | Dendritic cells | Secretion | Cell walls | MAP kinase | 1-Phosphatidylinositol 3-kinase | Dextran | Monocytes | Protein kinase | Interleukin 10 | Sepsis | Interferon | Colitis | Monocyte chemoattractant protein 1 | Cancer
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 04/2005, Volume 280, Issue 17, pp. 17286 - 17293
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 02/2015, Volume 125, Issue 2, pp. 665 - 680
Cellular lipid metabolism has been linked to immune responses; however, the precise mechanisms by which de novo fatty acid synthesis can regulate inflammatory... 
MEDICINE, RESEARCH & EXPERIMENTAL | OXIDATIVE STRESS | GLUCOSE-METABOLISM | ATP-CITRATE LYASE | UCP2 | SEPTIC SHOCK | CELL-GROWTH | CRITICALLY-ILL PATIENTS | INTENSIVE INSULIN THERAPY | CANCER | MITOCHONDRIAL UNCOUPLING PROTEINS | Fatty Acid Synthase, Type I - genetics | Fatty Acid Synthase, Type I - biosynthesis | Lipids - genetics | Inflammasomes - metabolism | NLR Family, Pyrin Domain-Containing 3 Protein | Humans | Ion Channels - genetics | Caspase 1 - metabolism | Mitochondrial Proteins - genetics | Interleukin-1beta - genetics | Lipids - biosynthesis | Sepsis - pathology | Interleukin-1beta - metabolism | Mitochondrial Proteins - metabolism | Sepsis - metabolism | Macrophages - pathology | Down-Regulation - genetics | Inflammasomes - genetics | Sepsis - genetics | Mice, Knockout | Carrier Proteins - genetics | Enzyme Induction - genetics | Macrophages - metabolism | Animals | Carrier Proteins - metabolism | Sepsis - chemically induced | Ion Channels - metabolism | Caspase 1 - genetics | Sepsis - therapy | Mice | Uncoupling Protein 2 | Interleukin-18 - genetics | Interleukin-18 - metabolism | Cellular proteins | Immune response | Synthesis | Sepsis | Development and progression | Lipids | Genetic aspects | Properties | Enzymes | Cytokines | Pathogenesis | Mortality | Glucose | Metabolism | Gene expression | Fatty acids | Proteins | Studies | Metabolites | Consent | Rodents
Journal Article
International Journal of Molecular Sciences, ISSN 1661-6596, 09/2017, Volume 18, Issue 9, p. 1932
Sepsis induces a wide range of effects on the red blood cell (RBC). Some of the effects including altered metabolism and decreased 2,3-bisphosphoglycerate are... 
Erythrocyte | Morphology and microcirculation | Sepsis | Rheology | RAT SKELETAL-MUSCLE | morphology and microcirculation | OXIDATIVE STRESS | rheology | INTRACELLULAR CALCIUM HOMEOSTASIS | BIOCHEMISTRY & MOLECULAR BIOLOGY | IN-VIVO P50 | DEPENDENT HYPOXIC VASODILATION | CHEMISTRY, MULTIDISCIPLINARY | erythrocyte | RESPIRATORY-DISTRESS-SYNDROME | SEPTIC SHOCK | RED-BLOOD-CELL | HYDROGEN-PEROXIDE | CRITICALLY-ILL PATIENTS | sepsis | Oxidative Stress | Calcium - metabolism | Antioxidants - metabolism | Humans | Critical Illness | Erythrocyte Indices | Oxygen - metabolism | Microcirculation | Sepsis - pathology | Sepsis - metabolism | Adenosine Triphosphate - metabolism | Cell Shape | Erythrocytes - pathology | Membrane Proteins - metabolism | 2,3-Diphosphoglycerate - metabolism | Neutrophils - metabolism | Disease Models, Animal | Oxidation-Reduction | Cell Survival | Endothelial Cells - metabolism | Erythrocyte Membrane - metabolism | Hemoglobins - metabolism | Cell Size | Animals | Erythrocytes - metabolism | Protein Binding | Virulence Factors - metabolism | Erythrocyte Deformability | Sepsis - blood | Sepsis - microbiology | Efflux | Deformability | Calcium (intracellular) | Deformation mechanisms | Virulence | Blood cells | Erythrocytes | Homeostasis | Formability | Phospholipids | Metabolism | Membrane proteins | Antioxidants | Proteins | Autoxidation | Virulence factors | Hemoglobin | Hypoxia | Bacteria | Microvasculature | ATP | Adenosine triphosphate | Calcium homeostasis
Journal Article