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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
Journal Article
Circulation: Cardiovascular Imaging, ISSN 1941-9651, 05/2013, Volume 6, Issue 3, pp. 363 - 372
Background-Although the recent surgical treatment of ischemic heart failure substudy reported that revascularization of viable myocardium did not improve... 
Prognosis | Ischemia | Positron emission tomography | Viability | Revascularization | HEART-RATE RECOVERY | SURVIVAL | revascularization | CARDIAC & CARDIOVASCULAR SYSTEMS | METAANALYSIS | CARDIOLOGY | VALIDATION | prognosis | EMISSION COMPUTED-TOMOGRAPHY | EXERCISE | ischemia | viability | MEDICAL THERAPY | positron emission tomography | RADIOLOGY, NUCLEAR MEDICINE & MEDICAL IMAGING | CORONARY-ARTERY-DISEASE | Predictive Value of Tests | Ventricular Function, Left | Humans | Middle Aged | Male | Positron-Emission Tomography | Ventricular Dysfunction, Left - mortality | Recovery of Function | Patient Selection | Ventricular Dysfunction, Left - therapy | Time Factors | Ventricular Dysfunction, Left - pathology | Myocardial Ischemia - diagnostic imaging | Myocardial Ischemia - physiopathology | Female | Myocardial Ischemia - mortality | Myocardial Stunning - diagnostic imaging | Radiopharmaceuticals | Rubidium Radioisotopes | Myocardial Revascularization - mortality | Myocardial Stunning - physiopathology | Risk Assessment | Risk Factors | Proportional Hazards Models | Myocardial Stunning - therapy | Myocardium - pathology | Treatment Outcome | Chi-Square Distribution | Myocardial Stunning - mortality | Ventricular Dysfunction, Left - diagnostic imaging | Ventricular Dysfunction, Left - physiopathology | Myocardial Ischemia - pathology | Myocardial Perfusion Imaging - methods | Myocardial Stunning - pathology | Stroke Volume | Cardiovascular Agents - therapeutic use | Propensity Score | Myocardial Ischemia - therapy | Fluorodeoxyglucose F18 | Tissue Survival | Aged | Hemodynamics | Myocardial Revascularization - adverse effects | Index Medicus
Journal Article
Journal Article
European Heart Journal, ISSN 0195-668X, 2017, Volume 38, Issue 45, pp. 3351 - 3358
Aims In patients with aortic stenosis (AS), risk stratification for aortic valve replacement (AVR) relies mainly on valverelated factors, symptoms and... 
Aortic stenosis | Transcatheter aortic valve implantation | Staging | Classification | Aortic valve replacement | Aortic valve | Transcatheter aortic valve replacement | CARDIAC & CARDIOVASCULAR SYSTEMS | RISK STRATIFICATION | PRESERVED EJECTION FRACTION | PROGNOSTIC VALUE | TRANSCATHETER | RIGHT-VENTRICULAR DYSFUNCTION | LOW-FLOW | LONGITUDINAL STRAIN | VALVE-REPLACEMENT | OUTCOMES | SEVERITY | Prognosis | Humans | Male | Ventricular Dysfunction, Left - mortality | Aortic Valve Stenosis - mortality | Activities of Daily Living | Hypertrophy, Left Ventricular - pathology | Ventricular Dysfunction, Left - pathology | Aged, 80 and over | Female | Aortic Valve Stenosis - surgery | Retrospective Studies | Aortic Valve Stenosis - classification | Hypertension, Pulmonary - mortality | Hypertrophy, Left Ventricular - mortality | Echocardiography | Risk Assessment | Hypertrophy, Left Ventricular - etiology | Ventricular Dysfunction, Left - etiology | Ventricular Dysfunction, Right - mortality | Ventricular Dysfunction, Right - etiology | Transcatheter Aortic Valve Replacement - statistics & numerical data | Transcatheter Aortic Valve Replacement - mortality | Hypertension, Pulmonary - etiology | Hypertension, Pulmonary - pathology | Ventricular Dysfunction, Right - pathology | Index Medicus | Editor's Choice | Fast Track | Fast Track Clinical Research
Journal Article
Circulation, ISSN 0009-7322, 07/2014, Volume 130, Issue 5, pp. 419 - 430
Journal Article
Circulation, ISSN 0009-7322, 03/2007, Volume 115, Issue 11, pp. 1398 - 1407
Background-Pressure overload is accompanied by cardiac myocyte apoptosis, hypertrophy, and inflammatory/fibrogenic responses that lead to ventricular... 
Heart failure | Hypertension | Cardiomyopathy | Inflammation | Metalloproteinases | Remodeling | Hypertrophy | heart failure | remodeling | SIGNALING PATHWAYS | CARDIAC & CARDIOVASCULAR SYSTEMS | TGF-BETA | hypertrophy | HEART-FAILURE | metalloproteinases | MECHANISMS | DILATED CARDIOMYOPATHY | inflammation | PROTEIN EXPRESSION | DISEASE | PERIPHERAL VASCULAR DISEASE | ADULT FELINE MYOCARDIUM | cardiomyopathy | HEMATOLOGY | hypertension | MATRIX-METALLOPROTEINASE INHIBITION | Myocardium - immunology | Tumor Necrosis Factor-alpha - genetics | Male | RNA, Messenger - metabolism | Matrix Metalloproteinase 9 - metabolism | Hypertrophy, Left Ventricular - pathology | Ventricular Pressure - physiology | Ventricular Dysfunction, Left - pathology | Aorta | Myocarditis - immunology | Disease Models, Animal | Myocytes, Cardiac - cytology | Mice, Inbred C57BL | Cells, Cultured | Myocardium - pathology | Ventricular Remodeling - physiology | Ventricular Dysfunction, Left - immunology | Ventricular Dysfunction, Left - physiopathology | Mice, Knockout | Hypertrophy, Left Ventricular - immunology | Animals | Myocytes, Cardiac - physiology | Fibrosis | Tumor Necrosis Factor-alpha - physiology | Mice | Hypertrophy, Left Ventricular - physiopathology | Myocarditis - pathology | Myocarditis - physiopathology | Apoptosis | Index Medicus | Abridged Index Medicus
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
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
Basic Research in Cardiology, ISSN 0300-8428, 9/2017, Volume 112, Issue 5, pp. 1 - 14
Advanced glycation end-products (AGEs) have been associated with poorer outcomes after myocardial infarction (MI), and linked with heart failure. Methylglyoxal... 
Myocardial infarction | Methylglyoxal | Advanced glycation end-products | Medicine & Public Health | Extracellular matrix | Bone marrow cells | Glyoxalase-1 | Cardiology | CELLS | APOPTOSIS | CARDIAC & CARDIOVASCULAR SYSTEMS | MYOCARDIAL-INFARCTION | HEART-FAILURE | BONE-MARROW | DIABETIC CARDIOMYOPATHY | ENDPRODUCTS AGES | DISEASE | MICE | EXPRESSION | Ventricular Function, Left | Humans | Lactoylglutathione Lyase - genetics | Ornithine - analogs & derivatives | Stem Cells - metabolism | Pyruvaldehyde - metabolism | Ventricular Remodeling | Time Factors | Myocardial Infarction - pathology | Myocardium - metabolism | Ventricular Dysfunction, Left - pathology | Myocardial Infarction - physiopathology | Disease Models, Animal | Imidazoles - metabolism | Genetic Predisposition to Disease | Collagen Type I - metabolism | Signal Transduction | Lactoylglutathione Lyase - metabolism | Ornithine - metabolism | Mice, Inbred C57BL | Cells, Cultured | Mice, Transgenic | Myocardium - pathology | Myocardial Infarction - metabolism | Ventricular Dysfunction, Left - physiopathology | Ventricular Dysfunction, Left - prevention & control | Ventricular Dysfunction, Left - metabolism | Phenotype | Animals | Glycation End Products, Advanced - metabolism | Stem Cells - pathology | Human Umbilical Vein Endothelial Cells - pathology | Myocardial Infarction - prevention & control | Neovascularization, Physiologic | Apoptosis | Immunohistochemistry | Heart | Enzymes | Collagen | Genetic engineering | Mass spectrometry | Cells | Heart attack | Cell culture | Collagen (type I) | Heart attacks | Arterioles | Remodeling | Damage prevention | Recruitment | Angiogenesis | Rodents | Cell adhesion | Bone marrow | Heart diseases | Age | Advanced glycosylation end products | Transgenic mice | Mass spectroscopy | Glycosylation | c-Kit protein | Overexpression | Stem cells | Cells (biology) | Myocardium | Mice | Infarction | Pyruvaldehyde | In vitro methods and tests | Index Medicus
Journal Article