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PLoS ONE, ISSN 1932-6203, 01/2014, Volume 9, Issue 1, p. e87936
The growing incidence of chronic kidney disease remains a global health problem. Obesity is a major risk factor for type-2 diabetes and renal impairment.... 
CHRONIC HEART-FAILURE | TISSUE INFLAMMATION | ATRIAL-NATRIURETIC-PEPTIDE | WAIST CIRCUMFERENCE | GLUCOSE-METABOLISM | MULTIDISCIPLINARY SCIENCES | IN-VIVO | ENHANCES INSULIN SENSITIVITY | FACTOR-KAPPA-B | CHRONIC KIDNEY-DISEASE | HYPERTENSIVE-RATS | Tumor Necrosis Factor-alpha - metabolism | Atrial Natriuretic Factor - metabolism | Endothelin-1 - metabolism | Diabetic Nephropathies - metabolism | Rats | Male | Dinoprost - metabolism | Interleukins - metabolism | Hemin - metabolism | Rats, Zucker | Inflammation - metabolism | Kidney - metabolism | Macrophages - metabolism | Animals | Diabetic Nephropathies - physiopathology | Chemokine CCL3 - metabolism | Adiposity - physiology | Dinoprost - analogs & derivatives | Blood Glucose - metabolism | Heme Oxygenase (Decyclizing) - metabolism | Extracellular Matrix Proteins - metabolism | Kidney - physiopathology | Inflammation - physiopathology | Type 2 diabetes | Adipose tissues | Fibronectins | Obesity | Endothelin | Cytokines | Diabetic nephropathies | Macrophages | Risk factors | Glucose metabolism | Chronic kidney failure | Collagen | Heme | Natriuretic peptides | Adipose tissue | Syngeneic grafts | Selectivity | Adipocytes | Fibronectin | Proteins | Genotype & phenotype | Cyclic GMP | Fibroblasts | Physiology | Carbon monoxide | Public health | Pulmonary arteries | Endothelin 1 | Tumor necrosis factor-α | Metabolism | Gene expression | Studies | Oxygenase | Hemin | Nephropathy | Fibrosis | Interleukin 10 | Infiltration | Renal function | Paracrine signalling | Adiponectin | Interleukin 6 | Rodents | Diaphragm (anatomy) | Extracellular matrix | Tumor necrosis factor-TNF | Lesions | Inducers | Creatinine | Hypertension | Excretion | Kidneys | Diabetes mellitus | Markers | Health risks | Inflammation | Morbidity | Scaffolding | Insulin resistance | Diaphragm | Diabetes | Proteinuria
Journal Article
Blood, ISSN 0006-4971, 2013, Volume 122, Issue 15, pp. 2757 - 2764
Journal Article
Circulation Research, ISSN 0009-7330, 04/2012, Volume 110, Issue 9, pp. 1217 - 1225
RATIONALE:The function of Nox4, a source of vascular H2O2, is unknown. Other Nox proteins were identified as mediators of endothelial dysfunction. OBJECTIVE:We... 
Hypertension | Angiogenesis | Carbon monoxide | Nitric oxide | Redox regulation | INDUCED ACTIVATION | nitric oxide | CARDIAC & CARDIOVASCULAR SYSTEMS | redox regulation | angiogenesis | carbon monoxide | ANGIOTENSIN-II | BLOOD-PRESSURE | NAD(P)H OXIDASE | ENDOTHELIAL-CELLS | IN-VIVO | CARDIOVASCULAR-DISEASE | PERIPHERAL VASCULAR DISEASE | SMOOTH-MUSCLE-CELLS | HYDROGEN-PEROXIDE | HEMATOLOGY | hypertension | UP-REGULATION | Catalase - pharmacology | Heme Oxygenase-1 - metabolism | Humans | NADPH Oxidases - metabolism | Male | Ischemia - genetics | Carbonates - pharmacology | RNA, Messenger - metabolism | NADPH Oxidases - deficiency | Time Factors | NADPH Oxidases - genetics | Carbonates - metabolism | Hemin - pharmacology | Hypertension - enzymology | Hypertension - genetics | Ischemia - pathology | Cytoprotection | Disease Models, Animal | Muscle, Skeletal - blood supply | NADH, NADPH Oxidoreductases - genetics | Hypertension - pathology | Hydrogen Peroxide - metabolism | Mice, Knockout | Human Umbilical Vein Endothelial Cells - enzymology | Organometallic Compounds - metabolism | Mice | Oxidative Stress - drug effects | Endothelial Cells - pathology | Endothelial Cells - enzymology | Hypertrophy | Ischemia - enzymology | Boranes - metabolism | Transfection | NADH, NADPH Oxidoreductases - deficiency | Hypertension - chemically induced | NF-E2-Related Factor 2 - genetics | Membrane Proteins - metabolism | Nitric Oxide Synthase Type III - metabolism | Angiotensin II | Polyethylene Glycols - pharmacology | Carbon Dioxide - metabolism | Mice, Inbred C57BL | Cells, Cultured | Boranes - pharmacology | Antioxidants - pharmacology | Ischemia - physiopathology | NADPH Oxidase 4 | Hypertension - physiopathology | NADPH Oxidase 1 | Animals | Lung - blood supply | Neovascularization, Physiologic | Organometallic Compounds - pharmacology | Apoptosis | Endothelial Cells - drug effects
Journal Article
Journal of Molecular and Cellular Cardiology, ISSN 0022-2828, 2010, Volume 49, Issue 2, pp. 186 - 195
Abstract Heme oxygenase-1 (HO-1) is highly protective in various pathophysiological states such as cardiovascular and neurodegenerative diseases. HO-1-derived... 
Cardiovascular | Peroxynitrite | Human umbilical vein endothelial cells | Hydrogen peroxide | Hemin | Biliverdin | Heme oxygenase-1 | Lipopolysaccharide | Biliverdin reductase | Superoxide | Bilirubin | NADPH OXIDASE | OXIDATIVE STRESS | ACTIVATION | CARDIAC & CARDIOVASCULAR SYSTEMS | MAJOR PHYSIOLOGICAL CYTOPROTECTANT | CELL BIOLOGY | HEART | CARDIOVASCULAR INJURY | CARBON-MONOXIDE | OXYGENASE | DYSFUNCTION | UP-REGULATION | Heme Oxygenase-1 - metabolism | Bilirubin - metabolism | Gene Silencing - drug effects | Reactive Oxygen Species - metabolism | Antioxidants - metabolism | Humans | Gene Knockdown Techniques | Respiratory Burst - drug effects | Cytoprotection - drug effects | Neutrophils - metabolism | Umbilical Veins - cytology | Xanthine Oxidase - metabolism | Angiotensin II - pharmacology | Free Radical Scavengers - metabolism | Neutrophils - drug effects | Biliverdine - metabolism | Mitochondria - metabolism | Mitochondria - drug effects | Oxidoreductases Acting on CH-CH Group Donors - metabolism | Tyrosine - metabolism | Endothelial Cells - cytology | Models, Biological | Nitrosation - drug effects | Lipopolysaccharides - pharmacology | Peroxynitrous Acid - metabolism | Leukocytes - drug effects | Endothelial Cells - enzymology | Leukocytes - metabolism | Endothelial Cells - drug effects | Oxidases | Nervous system diseases | Albumin | Endothelium | Antioxidants | Molybdenum compounds | Heterocyclic compounds | Analysis | Heme | Dihydrofolate reductase | Mitogens
Journal Article
Journal of Cellular Physiology, ISSN 0021-9541, 03/2010, Volume 222, Issue 3, pp. 757 - 768
Heme‐oxygenase‐1 (HO‐1), an important enzyme involved in vascular disease, transplantation, and inflammation, catalyzes the degradation of heme into carbon... 
OXIDATIVE STRESS | PHYSIOLOGY | CARBON-MONOXIDE | PROTEIN-KINASE | IN-VIVO | GENE-EXPRESSION | TNF-ALPHA | KAPPA-B | BONE | DIFFERENTIATION | LIVER-DISEASE | CELL BIOLOGY | Up-Regulation | Heme Oxygenase-1 - metabolism | Bilirubin - metabolism | Oxidative Stress | Diabetes Mellitus, Experimental - enzymology | Humans | Alkaline Phosphatase - metabolism | Male | Phosphatidylinositol 3-Kinases - metabolism | RNA, Messenger - metabolism | Core Binding Factor Alpha 1 Subunit - metabolism | Cell Differentiation - genetics | Heme Oxygenase-1 - genetics | Time Factors | Prostaglandin D2 - metabolism | Inflammation Mediators - metabolism | Prostaglandin D2 - analogs & derivatives | Membrane Proteins - metabolism | Hemin - pharmacology | Heme Oxygenase (Decyclizing) - metabolism | Proto-Oncogene Proteins c-akt - metabolism | Calcification, Physiologic - genetics | Carbon Dioxide - metabolism | Transduction, Genetic | Calcification, Physiologic - drug effects | Cytokines - metabolism | Osteoblasts - enzymology | Signal Transduction | Osteocalcin - metabolism | Osteoblasts - drug effects | Cells, Cultured | Hydrogen Peroxide - pharmacology | Rats | Iron - metabolism | Rats, Sprague-Dawley | Mice, Inbred ICR | Animals | Cell Differentiation - drug effects | Lipopolysaccharides - pharmacology | Mice | Organometallic Compounds - pharmacology | Mitogen-Activated Protein Kinases - metabolism
Journal Article
Journal Article
The EMBO Journal, ISSN 0261-4189, 07/2004, Volume 23, Issue 13, pp. 2544 - 2553
Bach1 is a transcriptional repressor of heme oxygenase‐1 and β‐globin genes, both of which are known to be transcriptionally induced by heme. To test the... 
heme oxygenase | Maf | globin | heme | oxidative stress | Globin | Oxidative stress | Heme | Heme oxygenase | CELLS | ACTIVATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | INDUCTION | OXYGENASE-1 GENE | LEUCINE ZIPPER PROTEIN | CELL BIOLOGY | CADMIUM | SMALL MAF | TRANSCRIPTION FACTOR NF-E2 | BINDING | Immunohistochemistry | Heme - metabolism | Transcription Factors - chemistry | Humans | Leucine Zippers | Molecular Sequence Data | Globins - metabolism | Recombinant Fusion Proteins - metabolism | DNA-Binding Proteins - metabolism | Cell Nucleus - metabolism | Chromatin Immunoprecipitation | Heme Oxygenase-1 | Transcription, Genetic | Active Transport, Cell Nucleus | Hemin - pharmacology | Heme Oxygenase (Decyclizing) - metabolism | Dimerization | Heme Oxygenase (Decyclizing) - genetics | Genes, Reporter | Repressor Proteins - metabolism | Fibroblasts - metabolism | Amino Acid Sequence | Cell Line | Green Fluorescent Proteins - metabolism | Zinc Fingers | Gene Expression Regulation | Glutathione Transferase - metabolism | Alanine - metabolism | Nuclear Proteins - metabolism | Recombinant Fusion Proteins - chemistry | Transcription Factors - genetics | Fanconi Anemia Complementation Group Proteins | Amino Acid Motifs | MafK Transcription Factor | Membrane Proteins | Transcription Factors - metabolism | Karyopherins - metabolism | Escherichia coli - genetics | Plasmids | Fibroblasts - drug effects | Erythroid-Specific DNA-Binding Factors | Spectrophotometry | Basic-Leucine Zipper Transcription Factors | Amino Acid Substitution | Receptors, Cytoplasmic and Nuclear - metabolism
Journal Article
Journal Article
NATURE, ISSN 0028-0836, 04/2019, Volume 568, Issue 7751, pp. 254 - 254
Mitochondrial metabolism is an attractive target for cancer therapy(1,2). Reprogramming metabolic pathways could improve the ability of metabolic inhibitors to... 
METFORMIN | REGULATOR | COMPLEX | NETWORK | METASTASIS | AVAILABILITY | MULTIDISCIPLINARY SCIENCES | TRANSCRIPTION | GENE-EXPRESSION | CELL SENSITIVITY | REVEALS | Basic-Leucine Zipper Transcription Factors - metabolism | Metformin - therapeutic use | Electron Transport - genetics | Humans | Metformin - metabolism | Triple Negative Breast Neoplasms - drug therapy | Hemin - metabolism | Heterografts | Mitochondria - genetics | Basic-Leucine Zipper Transcription Factors - deficiency | Proteolysis | Triple Negative Breast Neoplasms - pathology | Female | Basic-Leucine Zipper Transcription Factors - antagonists & inhibitors | Mitochondria - metabolism | Basic-Leucine Zipper Transcription Factors - genetics | Mitochondria - drug effects | Xenograft Model Antitumor Assays | Animals | Triple Negative Breast Neoplasms - genetics | Mice, Nude | Triple Negative Breast Neoplasms - metabolism | Glucose - metabolism | Citric Acid Cycle - physiology | Mice | Hemin - therapeutic use | Care and treatment | Mitochondria | Transcription factors | Physiological aspects | Breast cancer | Metabolism | Health aspects | Methods | Cancer | Tricarboxylic acid cycle | Dehydrogenases | Genomics | Xenotransplantation | Homology | Genomes | Kinases | Cancer therapies | Computer numerical control | Datasets | Electron transport chain | Glucose metabolism | Metabolites | Xenografts | Trends | Bioinformatics | Phenotypes | Haem | Gene expression | Ribonucleic acid--RNA | Patients | Depletion | Inhibitors | Hemin | Breast | Metabolic pathways | Metformin | Respiration | Electron transport | Binding sites | Tumors
Journal Article
Science, ISSN 0036-8075, 9/2004, Volume 305, Issue 5690, pp. 1626 - 1628