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Circulation Research, ISSN 0009-7330, 01/2009, Volume 104, Issue 2, pp. 210 - 218
Oxidative modification of low-density lipoprotein (LDL) plays a causative role in the development of atherosclerosis. In this study, we demonstrate that... 
Reactive oxygen species | Minimally oxidized LDL | RANTES | Atherosclerosis | NADPH oxidase 2 | atherosclerosis | AORTIC ENDOTHELIAL-CELLS | CARDIAC & CARDIOVASCULAR SYSTEMS | SYK | SUPEROXIDE-PRODUCTION | minimally oxidized LDL | CUTTING EDGE | NOX FAMILY | reactive oxygen species | LIPOPOLYSACCHARIDE | PERIPHERAL VASCULAR DISEASE | MICE | HEMATOLOGY | NF-KAPPA-B | Phosphorylation | Reactive Oxygen Species - metabolism | Membrane Glycoproteins - metabolism | Muscle, Smooth, Vascular - metabolism | Protein-Tyrosine Kinases - metabolism | NADPH Oxidases - metabolism | Intracellular Signaling Peptides and Proteins - metabolism | Gene Knockdown Techniques | NADPH Oxidases - deficiency | Atherosclerosis - enzymology | Time Factors | Toll-Like Receptor 4 - deficiency | Interleukin-1beta - metabolism | Protein Kinase C - metabolism | Inflammation Mediators - metabolism | NADPH Oxidases - genetics | Chemokine CCL5 - metabolism | Lipoproteins, LDL - metabolism | Interleukin-6 - metabolism | Myocytes, Smooth Muscle - metabolism | Syk Kinase | Cell Line | Phospholipase C gamma - metabolism | Atherosclerosis - immunology | Signal Transduction | Macrophages, Peritoneal - enzymology | Myeloid Differentiation Factor 88 - genetics | Macrophages, Peritoneal - immunology | Toll-Like Receptor 4 - genetics | NADPH Oxidase 2 | Toll-Like Receptor 4 - metabolism | Membrane Glycoproteins - genetics | Mice, Knockout | Animals | Mice | Enzyme Activation | Myeloid Differentiation Factor 88 - metabolism | Membrane Glycoproteins - deficiency | Cell Movement | Index Medicus
Journal Article
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 | Index Medicus
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 8/2010, Volume 107, Issue 35, pp. 15565 - 15570
NAD(P)H oxidases (Noxs) produce O 2 − and play an important role in cardiovascular pathophysiology. The Nox4 isoform is expressed primarily in the mitochondria... 
Heart | Oxidases | Oxidative stress | Cardiomegaly | Up regulation | Mitochondria | Transcriptional regulatory elements | Reactive oxygen species | Fibrosis | Apoptosis | Cardiac hypertrophy | Superoxide | NAD(P)H oxidase | MYOCARDIUM | PRESSURE-OVERLOAD | MYOCYTES | mitochondria | MULTIDISCIPLINARY SCIENCES | FAILURE | MITOCHONDRIAL PERMEABILITY TRANSITION | CARDIAC-HYPERTROPHY | RADICALS | cardiac hypertrophy | superoxide | REVEALS | Reactive Oxygen Species - metabolism | Oxidative Stress | NADPH Oxidases - metabolism | Immunoblotting | Male | Isoenzymes - metabolism | Myocardium - metabolism | NADPH Oxidases - genetics | Female | Heart - physiopathology | In Situ Nick-End Labeling | Echocardiography | Isoenzymes - genetics | Mice, Inbred C57BL | Cardiomegaly - physiopathology | Heart Failure - genetics | Myocardium - pathology | Heart Failure - metabolism | Mitochondria - metabolism | Heart Failure - pathology | NADPH Oxidase 4 | Reverse Transcriptase Polymerase Chain Reaction | Mice, Knockout | Myocytes, Cardiac - pathology | Animals | Myocytes, Cardiac - metabolism | Mice | Cardiomegaly - genetics | Mitochondria - physiology | Cardiomegaly - metabolism | Heart failure | Composition | Genetic aspects | Health aspects | Proteins | Genotype & phenotype | Rodents | Cardiomyocytes | Physiology | Gene expression | Index Medicus | Biological Sciences
Journal Article
Journal Article
Nature Cell Biology, ISSN 1465-7392, 07/2015, Volume 17, Issue 7, pp. 893 - 906
LC3-associated phagocytosis (LAP) is a process wherein elements of autophagy conjugate LC3 to phagosomal membranes. We characterize the molecular requirements... 
NONCANONICAL AUTOPHAGY | REGULATE AUTOPHAGY | IMMUNITY | CROHN-DISEASE | INFLAMMATION | MICE | NADPH OXIDASE ACTIVATION | CELLULAR DEFENSE | BINDING | GENOME-WIDE ASSOCIATION | CELL BIOLOGY | Phagosomes - microbiology | Autophagy-Related Proteins | Phosphatidylinositol Phosphates - metabolism | Reactive Oxygen Species - metabolism | Membrane Glycoproteins - metabolism | Microtubule-Associated Proteins - genetics | Microtubule-Associated Proteins - metabolism | Vesicular Transport Proteins - metabolism | NADPH Oxidases - metabolism | Immunoblotting | Male | Green Fluorescent Proteins - genetics | Intracellular Signaling Peptides and Proteins - metabolism | Autophagy | RNA Interference | Tumor Suppressor Proteins - genetics | Aspergillus fumigatus - physiology | NADPH Oxidases - genetics | Female | Intracellular Signaling Peptides and Proteins - genetics | Macrophages - microbiology | Cell Line | Green Fluorescent Proteins - metabolism | Tumor Suppressor Proteins - metabolism | Mice, Inbred C57BL | Phagosomes - metabolism | Vesicular Transport Proteins - genetics | Class III Phosphatidylinositol 3-Kinases - metabolism | Mice, Transgenic | NADPH Oxidase 2 | Membrane Glycoproteins - genetics | Mice, Knockout | Host-Pathogen Interactions | Microscopy, Confocal | Macrophages - metabolism | Animals | Phagocytosis | Cellular proteins | Development and progression | Genetic aspects | Properties | Communicable diseases | Index Medicus
Journal Article
PLoS ONE, ISSN 1932-6203, 07/2015, Volume 10, Issue 7, pp. e0129743 - e0129743
Reactive oxygen species (ROS) produced by nicotinamide adenine dinucleotide phosphate oxidase (NOX) play a key role in liver injury and fibrosis. Previous... 
TRANSFORMATION | NADPH OXIDASE | HEPATOCYTE APOPTOSIS | OXIDATIVE STRESS | SIGNALING PATHWAYS | HEDGEHOG PATHWAY | MULTIDISCIPLINARY SCIENCES | INVOLVEMENT | NAD(P)H OXIDASES | PROLIFERATION | EXPRESSION | NADPH Oxidases - chemistry | Reactive Oxygen Species - metabolism | Humans | NADPH Oxidases - metabolism | Hedgehog Proteins - metabolism | Hepatic Stellate Cells - metabolism | Platelet-Derived Growth Factor - genetics | Myofibroblasts - metabolism | Carbon Tetrachloride Poisoning - metabolism | Hedgehog Proteins - genetics | Hepatitis - genetics | Hepatitis - metabolism | Liver Cirrhosis - metabolism | NADPH Oxidases - genetics | NADH, NADPH Oxidoreductases - metabolism | Liver Cirrhosis - genetics | Hepatic Stellate Cells - pathology | Myofibroblasts - pathology | NADH, NADPH Oxidoreductases - genetics | Signal Transduction | NADPH Oxidases - antagonists & inhibitors | Hepatitis - pathology | NADPH Oxidase 4 | Pyrazoles - metabolism | Carbon Tetrachloride Poisoning - pathology | NADPH Oxidase 1 | Mice, Knockout | Platelet-Derived Growth Factor - metabolism | Animals | Pyridines - metabolism | Liver Cirrhosis - pathology | Carbon Tetrachloride Poisoning - genetics | Mice | NADH, NADPH Oxidoreductases - antagonists & inhibitors | Niacinamide | Platelet-derived growth factor | Carbon tetrachloride | Fibrosis | Inflammation | Comparative analysis | Liver cirrhosis | Phosphates | Oxidative stress | Pathogenesis | Liver | Genes | Lipid peroxidation | Activation | NAD(P)H oxidase | Lipopolysaccharides | Veterinarians | Hepatitis | Cell activation | NOX4 protein | Rodents | Cell cycle | Peroxidation | Medical research | Stellate cells | Enzymes | NADPH-diaphorase | Adenine | CCL4 protein | Medicine | Cirrhosis | Signaling | Injury prevention | Inhibitors | Hedgehog protein | Nicotinamide adenine dinucleotide | Nicotinamide | Laboratory animals | Plastics | Apoptosis | Bile | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 10/2011, Volume 478, Issue 7368, pp. 264 - 268
Journal Article
Journal Article