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Circulation Research, ISSN 0009-7330, 04/2010, Volume 106, Issue 7, pp. 1253 - 1264
RATIONALE:NADPH oxidases are a major source of superoxide (O2) in the cardiovascular system. The function of Nox4, a member of the Nox family of NADPH... 
Aging | Oxidative stress | Reactive oxygen species | Superoxide | Apoptosis | Hypertrophy | CELLS | PRESSURE-OVERLOAD | CARDIAC & CARDIOVASCULAR SYSTEMS | hypertrophy | PHOSPHORYLATION | apoptosis | ANGIOTENSIN-II | FAMILY NADPH OXIDASES | FREE-RADICALS | NAD(P)H OXIDASE | reactive oxygen species | PERIPHERAL VASCULAR DISEASE | GENERATION | aging | superoxide | HEMATOLOGY | oxidative stress | Aconitate Hydratase - metabolism | Up-Regulation | Cysteine | Cell Proliferation | Uncoupling Agents - pharmacology | Oxidative Stress | Rats, Wistar | Ventricular Function, Left | Apoptosis - drug effects | Mitochondria, Heart - pathology | Humans | NADPH Oxidases - metabolism | Cardiomegaly - pathology | Mitochondria, Heart - drug effects | Myocytes, Cardiac - enzymology | Transfection | Ventricular Dysfunction, Left - genetics | Rotenone - pharmacology | Superoxides - metabolism | Ventricular Dysfunction, Left - pathology | NADPH Oxidases - genetics | Ventricular Dysfunction, Left - enzymology | Disease Models, Animal | Oxidation-Reduction | NADPH Oxidases - antagonists & inhibitors | Cells, Cultured | Enzyme Inhibitors - pharmacology | Mitochondria, Heart - enzymology | Cardiomegaly - physiopathology | Rats | Genotype | Mice, Transgenic | Cardiomegaly - enzymology | NADPH Oxidase 4 | Onium Compounds - pharmacology | NADH Dehydrogenase - metabolism | Ventricular Dysfunction, Left - physiopathology | Aging - pathology | Myocytes, Cardiac - pathology | Phenotype | Animals | Myocytes, Cardiac - drug effects | Fibrosis | Mice | Cardiomegaly - genetics | Aging - metabolism | Index Medicus
Journal Article
Journal of the American College of Cardiology, ISSN 0735-1097, 06/2014, Volume 63, Issue 24, pp. 2734 - 2741
Objectives This study sought to investigate the effect of endothelial dysfunction on the development of cardiac hypertrophy and fibrosis. Background... 
Cardiovascular | Internal Medicine | endothelial-mesenchymal transition | diastolic dysfunction | endothelium | NADPH (nicotinamide adenine dinucleotide phosphate) oxidase | angiotensin II | CELLS | OXIDATIVE STRESS | CARDIAC & CARDIOVASCULAR SYSTEMS | ANGIOGENESIS | HEART-FAILURE | ATHEROSCLEROSIS | ANGIOTENSIN-II | PATHOPHYSIOLOGY | HYPERTROPHY | MICE | CONTRIBUTES | Heart Failure, Diastolic - genetics | Mesenchymal Stromal Cells - enzymology | Humans | Cardiomegaly - pathology | Male | Endothelium, Vascular - enzymology | Membrane Glycoproteins - physiology | Ventricular Dysfunction, Left - genetics | Ventricular Dysfunction, Left - pathology | NADPH Oxidases - genetics | Ventricular Dysfunction, Left - enzymology | Inflammation Mediators - physiology | Fibrosis - genetics | Fibrosis - enzymology | Cells, Cultured | Heart Failure, Diastolic - enzymology | Mice, Transgenic | Cardiomegaly - enzymology | Heart Failure, Diastolic - pathology | NADPH Oxidase 2 | Membrane Glycoproteins - genetics | Animals | Endothelium, Vascular - pathology | Mice | Fibrosis - pathology | Mesenchymal Stromal Cells - pathology | Cardiomegaly - genetics | NADPH Oxidases - physiology | Oxidases | Heart | Fibrosis | Stem cells | Endothelium | Hypertension | Heart failure | Genotype & phenotype | Stroke | Heart attacks | Pathogenesis | Rodents | Cardiomyocytes | Variance analysis | Index Medicus | Abridged Index Medicus
Journal Article
Cardiovascular Research, ISSN 0008-6363, 12/2012, Volume 96, Issue 3, pp. 444 - 455
Age-related diastolic dysfunction has been attributed to an increased passive stiffness, which is regulated by extracellular matrix (ECM). We recently showed... 
Diastolic function | Extracellular matrix | Matrix metalloproteinase | Ageing | Collagen | CARDIAC & CARDIOVASCULAR SYSTEMS | TGF-BETA | ANGIOGENESIS | PROTECTION | HEART-FAILURE | FIBROBLASTS | MATRIX METALLOPROTEINASES | CARDIAC-HYPERTROPHY | PERIOSTIN EXPRESSION | REVEALS | Blood Pressure | Cell Adhesion Molecules - genetics | Phosphorylation | Age Factors | Diastole | Ventricular Function, Left | Male | Systole | Ventricular Dysfunction, Left - genetics | Matrix Metalloproteinase 8 - metabolism | Matrix Metalloproteinase 9 - genetics | Smad2 Protein - genetics | Ventricular Dysfunction, Left - pathology | Ventricular Dysfunction, Left - enzymology | Female | Real-Time Polymerase Chain Reaction | Matrix Metalloproteinase 8 - genetics | Signal Transduction | Mice, Inbred C57BL | Gene Expression Regulation | Smad2 Protein - metabolism | Ventricular Dysfunction, Left - etiology | Genotype | Myocardium - pathology | Matrix Metalloproteinase 9 - deficiency | Cell Adhesion Molecules - metabolism | Ventricular Dysfunction, Left - physiopathology | Ventricular Dysfunction, Left - prevention & control | Aging - pathology | Mice, Knockout | Collagen - metabolism | Myocardium - enzymology | Phenotype | Animals | Transforming Growth Factor beta - genetics | Fibrosis | Connective Tissue Growth Factor - genetics | Mice | Transforming Growth Factor beta - metabolism | Connective Tissue Growth Factor - metabolism | Aging - metabolism | Index Medicus | Original
Journal Article
PLoS ONE, ISSN 1932-6203, 12/2012, Volume 7, Issue 12, pp. e52013 - e52013
Objectives: Diabetic cardiomyopathy (DCM), characterized by myocardial structural and functional changes, is an independent cardiomyopathy that develops in... 
FIBROSIS | CELLS | OXIDATIVE STRESS | MULTIDISCIPLINARY SCIENCES | HEART-FAILURE | GENE-EXPRESSION | CARDIAC DYSFUNCTION | PPAR-GAMMA | RECEPTOR | GLYCATION END-PRODUCTS | DIASTOLIC DYSFUNCTION | Inflammation - pathology | Diabetes Mellitus, Experimental - drug therapy | Fibrosis - drug therapy | Diabetic Cardiomyopathies - metabolism | Diabetic Cardiomyopathies - drug therapy | Rats, Wistar | Apoptosis - drug effects | Diabetes Mellitus, Experimental - genetics | Apoptosis - genetics | Glycogen Synthase Kinase 3 beta | Male | Fibrosis - metabolism | Proto-Oncogene Proteins c-akt - genetics | Inflammation - metabolism | Cell Death - genetics | Ventricular Dysfunction, Left - genetics | Inflammation - drug therapy | Myocardium - metabolism | Ventricular Dysfunction, Left - pathology | Cell Death - drug effects | Phosphorylation - drug effects | Diabetes Mellitus, Experimental - metabolism | Proto-Oncogene Proteins c-akt - metabolism | Receptor for Advanced Glycation End Products | Fibrosis - genetics | Curcumin - pharmacology | Oxidative Stress - genetics | Rats | Myocardium - pathology | Glycogen Synthase Kinase 3 - metabolism | Diabetic Cardiomyopathies - genetics | Ventricular Dysfunction, Left - metabolism | Animals | Ventricular Dysfunction, Left - drug therapy | Glycogen Synthase Kinase 3 - genetics | Diabetes Mellitus, Experimental - pathology | Heart - drug effects | Inflammation - genetics | Diabetic Cardiomyopathies - pathology | Fibrosis - pathology | Oxidative Stress - drug effects | Receptors, Immunologic - genetics | Receptors, Immunologic - metabolism | Oxidases | Heart | Biological products | Cardiomyopathy | Heart diseases | Enzyme-linked immunosorbent assay | Apoptosis | Oxidative stress | Phosphorylation | Bax protein | Bcl-2 protein | Science | AKT protein | Cardiovascular disease | Caspase-3 | NAD(P)H oxidase | Accumulation | Proteins | Signal transduction | Hyperglycemia | Ultrastructure | Biochemical tests | Curcumin | Age | Energy intake | Stresses | Enzymes | Advanced glycosylation end products | Echocardiography | Abnormalities | Diabetes mellitus | Caspase | Rac1 protein | Pharmacology | Inflammation | Glycosylation | IL-1β | Gene expression | Metabolism | Stress | Studies | Signaling | Cell death | Fibrosis | Diabetes | Aberration | Laboratory animals | Metabolic disorders | Hypertrophy | Index Medicus
Journal Article
Hypertension, ISSN 0194-911X, 12/2015, Volume 66, Issue 6, pp. 1159 - 1167
Journal Article
American Journal of Physiology : Heart and Circulatory Physiology, ISSN 0363-6135, 2014, Volume 306, Issue 7, pp. H1025 - 31
Patients with heart failure (HF) have enhanced systemic IL-1 activity, and, in the experimental mouse model, IL-1 induces left ventricular (LV) systolic... 
Heart failure | Inflammation | Interleukins | Systolic dysfunction | heart failure | CARDIAC & CARDIOVASCULAR SYSTEMS | PHYSIOLOGY | CARDIOVASCULAR EVENTS | INCREASED CIRCULATING INTERLEUKIN-18 | MONONUCLEAR-CELLS | BINDING-PROTEIN | systolic dysfunction | NECROSIS-FACTOR-ALPHA | RECEPTOR ANTAGONIST | interleukins | inflammation | ACUTE MYOCARDIAL-INFARCTION | GENE-EXPRESSION | PERIPHERAL VASCULAR DISEASE | BLOCKING INTERLEUKIN-1 | CONGESTIVE-HEART-FAILURE | Humans | Heart Failure - physiopathology | Male | Systole | Heart Failure - blood | Ventricular Dysfunction, Left - chemically induced | Time Factors | Ventricular Dysfunction, Left - blood | Ventricular Dysfunction, Left - genetics | Interleukin-6 - blood | Interleukin 1 Receptor Antagonist Protein - pharmacology | Disease Models, Animal | Signal Transduction | Mice, Inbred C57BL | Ventricular Function, Left - drug effects | Interleukin-18 - deficiency | Heart Failure - genetics | Heart Failure - metabolism | Interleukin-1beta | Ventricular Dysfunction, Left - physiopathology | Mice, Knockout | Antibodies - pharmacology | Ventricular Dysfunction, Left - metabolism | Animals | Intercellular Signaling Peptides and Proteins - pharmacology | Mice | Interleukin-18 - genetics | Heart Failure - chemically induced | Interleukin-18 - metabolism | Cardiac patients | Physiological aspects | Research | Cardiovascular research | Health aspects | Protein-protein interactions | Plasma | Cytokines | Rodents | Index Medicus | Signaling and Stress Response
Journal Article
American Journal of Physiology - Heart and Circulatory Physiology, ISSN 0363-6135, 12/2009, Volume 297, Issue 6, pp. 2096 - 2108
Diabetic cardiomyopathy is an important contributor to diastolic and systolic heart failure. We examined the nature and mechanism of the cardiomyopathy in... 
Sarco(endo)plasmic reticulum calcium-ATPase 2a | Insulin | Fibrosis | Hypertrophy | OVERLOAD | PROTEIN-KINASE-C | OXIDATIVE STRESS | CARDIAC & CARDIOVASCULAR SYSTEMS | PHYSIOLOGY | insulin | MECHANISM | hypertrophy | HEART-FAILURE | CHRONIC ACTIVATION | sarco(endo)plasmic reticulum calcium-ATPase 2a | INSULIN-RESISTANCE | EJECTION FRACTION | PERIPHERAL VASCULAR DISEASE | fibrosis | MICE | EXPRESSION | Cardiomyopathies - diagnostic imaging | Mitochondria, Heart - metabolism | Age Factors | Diastole | Natriuretic Peptide, Brain - metabolism | Diabetes Mellitus, Type 1 - metabolism | Myocardial Contraction - drug effects | Male | Diabetes Mellitus, Type 1 - diagnostic imaging | Diabetes Mellitus, Type 1 - complications | Systole | Insulin - blood | Echocardiography, Doppler, Pulsed | Myosin Heavy Chains - metabolism | Cardiomyopathies - genetics | Cardiomyopathies - physiopathology | Diglycerides - metabolism | Ventricular Dysfunction, Left - genetics | Mice, Mutant Strains | Myocardium - metabolism | Lipid Metabolism - genetics | Insulin - genetics | Fatty Acids - metabolism | Protein-Serine-Threonine Kinases - metabolism | Disease Models, Animal | Cardiomyopathies - drug therapy | Insulin - pharmacology | Sarcoplasmic Reticulum Calcium-Transporting ATPases - metabolism | Ceramides - metabolism | Acyl-CoA Dehydrogenase, Long-Chain - metabolism | Diabetes Mellitus, Type 1 - physiopathology | Mice, Inbred C57BL | Diabetes Mellitus, Type 1 - genetics | Disease Progression | Ventricular Dysfunction, Left - diagnostic imaging | Ventricular Dysfunction, Left - physiopathology | Diabetes Mellitus, Type 1 - drug therapy | Hypoglycemic Agents - pharmacology | Triglycerides - metabolism | Stroke Volume | Ventricular Dysfunction, Left - metabolism | Animals | Ventricular Dysfunction, Left - drug therapy | Cardiomyopathies - metabolism | Lipid Metabolism - drug effects | Mice | Ventricular Pressure | Blood Glucose - metabolism | Heart failure | Complications and side effects | Prognosis | Cardiomyopathy | Type 1 diabetes | Heart diseases | Risk factors | Heart | Rodents | Oxidation | Glucose | Diabetes | Kinases | Index Medicus
Journal Article
Journal Article
Lancet, The, ISSN 0140-6736, 2010, Volume 375, Issue 9716, pp. 752 - 762
Journal Article
Journal Article