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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
Circulation Research, ISSN 0009-7330, 02/2013, Volume 112, Issue 4, pp. 675 - 688
RATIONALE:Matrix metalloproteinase (MMP)-28 regulates the inflammatory and extracellular matrix responses in cardiac aging, but the roles of MMP-28 after... 
fibroblast | MMP-28 | inflammation | macrophage phenotype | myocardial infarction | LYSYL OXIDASE | CARDIAC & CARDIOVASCULAR SYSTEMS | TGF-BETA | VENTRICULAR-FUNCTION | HEART-FAILURE | CORONARY MICROEMBOLIZATION | REPAIR | MATRIX-METALLOPROTEINASE-9 | PERIPHERAL VASCULAR DISEASE | EPILYSIN MMP-28 | TNF-ALPHA | TARGETED DELETION | HEMATOLOGY | Myocardial Infarction - blood | Cell Adhesion Molecules - genetics | Cicatrix - etiology | Extracellular Matrix Proteins - biosynthesis | Male | Matrix Metalloproteinases, Secreted - deficiency | Pulmonary Edema - etiology | Myocytes, Cardiac - enzymology | Myofibroblasts - metabolism | Ventricular Dysfunction, Left - enzymology | Ventricular Remodeling - genetics | Female | Myocardial Infarction - physiopathology | Transcription, Genetic | Cytokines - genetics | Heart Rupture - enzymology | Receptors, Cytokine - genetics | Matrix Metalloproteinase 9 - blood | Myocardial Infarction - enzymology | Macrophage Activation - physiology | Macrophages - classification | Cell Adhesion Molecules - biosynthesis | Receptors, Cytokine - biosynthesis | Extracellular Matrix Proteins - genetics | Mice, Inbred C57BL | Gene Expression Regulation | Ventricular Dysfunction, Left - etiology | Inflammation | Ventricular Remodeling - physiology | Macrophages - enzymology | Mice, Knockout | Collagen - metabolism | Myocardial Infarction - complications | Heart Rupture - etiology | Animals | Pulmonary Edema - enzymology | Matrix Metalloproteinases, Secreted - genetics | Matrix Metalloproteinases, Secreted - physiology | Protein-Lysine 6-Oxidase - metabolism | Cicatrix - enzymology | Mice | Cytokines - biosynthesis | Index Medicus
Journal Article
Antioxidants & Redox Signaling, ISSN 1523-0864, 01/2013, Volume 18, Issue 1, pp. 5 - 18
Journal Article
American Journal of Physiology - Heart and Circulatory Physiology, ISSN 0363-6135, 2017, Volume 313, Issue 2, pp. H224 - H236
Myocardial infarction (MI) results in loss of cardiomyocytes, adverse extracellular matrix (ECM) and structural remodeling, and left ventricular (LV) dilation... 
Remodeling | Tissue inhibitor of metalloproteinases 3 | remodeling | ACTIVATION | CARDIAC & CARDIOVASCULAR SYSTEMS | PHYSIOLOGY | tissue inhibitor of metalloproteinases 3 | POSTMYOCARDIAL INFARCTION | HEART-FAILURE | DIASTOLIC DYSFUNCTION | MATRIX METALLOPROTEINASES | DISINTEGRIN | TISSUE INHIBITOR | PERIPHERAL VASCULAR DISEASE | BIOMECHANICAL STRESS | MICE | WALL-MOTION SCORE | Myocardial Infarction - genetics | Up-Regulation | Cell Proliferation | Hypertrophy, Left Ventricular - enzymology | Ventricular Function, Left | Coronary Vessels - physiopathology | Humans | Male | Recovery of Function | Myocardial Infarction - therapy | Ventricular Remodeling | Hypertrophy, Left Ventricular - genetics | Time Factors | Ventricular Dysfunction, Left - genetics | Proteolysis | Tissue Inhibitor of Metalloproteinase-3 - biosynthesis | Adenoviridae - genetics | Ventricular Dysfunction, Left - enzymology | Myocardial Infarction - physiopathology | Disease Models, Animal | Myocardial Infarction - enzymology | Tissue Inhibitor of Metalloproteinase-3 - genetics | Coronary Vessels - enzymology | Transduction, Genetic | Signal Transduction | Hypertrophy, Left Ventricular - prevention & control | Mice, Inbred C57BL | Myocardium - pathology | Ventricular Dysfunction, Left - physiopathology | Ventricular Dysfunction, Left - prevention & control | Myocardium - enzymology | Animals | Adenoviridae - metabolism | Hypertrophy, Left Ventricular - physiopathology | Matrix Metalloproteinases - metabolism | Endothelial Cells - pathology | Genetic Vectors | Endothelial Cells - enzymology | Neovascularization, Physiologic | Genetic Therapy - methods | Angiogenesis | Protein expression | Heart attacks | Matrix | Effects | Rodents | Index Medicus
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 6/2011, Volume 108, Issue 23, pp. 9572 - 9577
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
Journal Article
Journal Article
Cardiovascular Research, ISSN 0008-6363, 2015, Volume 105, Issue 3, pp. 318 - 329
TNF-alpha (TNF-alpha) causes left ventricular diastolic dysfunction. Down-regulation of sarcoplasmic reticulum Ca2+-ATPase 2a protein (SERCA2a) expression is... 
Diastolic dysfunction | SERCA2a | TNF-α | Transcription | Simvastatin | Atp2a2 | APOPTOSIS | CARDIAC & CARDIOVASCULAR SYSTEMS | TNF-alpha | HEART-FAILURE | PRESERVED EJECTION FRACTION | CARDIOMYOCYTES | TUMOR-NECROSIS-FACTOR | INHIBITION | INFLAMMATION | atp2a2 | CARDIAC CONTRACTILITY | ROSUVASTATIN | MODULATION | Inflammation - chemically induced | Tumor Necrosis Factor-alpha - metabolism | Diastole | Rats, Wistar | Male | NF-kappa B - metabolism | Ventricular Dysfunction, Left - chemically induced | Lipopolysaccharides | Dose-Response Relationship, Drug | Myocytes, Cardiac - enzymology | Ventricular Dysfunction, Left - genetics | Ventricular Dysfunction, Left - enzymology | Transcription, Genetic | Binding Sites | Disease Models, Animal | Cell Line | Promoter Regions, Genetic | NF-kappa B - antagonists & inhibitors | Sarcoplasmic Reticulum Calcium-Transporting ATPases - metabolism | Signal Transduction | Anti-Inflammatory Agents - pharmacology | Down-Regulation | Ventricular Function, Left - drug effects | Ventricular Dysfunction, Left - physiopathology | Ventricular Dysfunction, Left - prevention & control | Gene Expression Regulation, Enzymologic | Tumor Necrosis Factor-alpha - pharmacology | Animals | Myocytes, Cardiac - drug effects | NF-kappa B - genetics | Inflammation - genetics | Protein Binding | Inflammation - prevention & control | Mice | Sarcoplasmic Reticulum Calcium-Transporting ATPases - genetics | Inflammation - enzymology | Inflammation - physiopathology | Index Medicus
Journal Article
Circulation, ISSN 0009-7322, 05/2009, Volume 119, Issue 19, pp. 2568 - 2577
Background-Some studies have shown that metformin activates AMP-activated protein kinase (AMPK) and has a potent cardioprotective effect against... 
Heart failure | Metformin | AMP-activated protein kinase | Nitric oxide | heart failure | nitric oxide | CARDIAC & CARDIOVASCULAR SYSTEMS | ENDOTHELIAL NO SYNTHASE | BLOOD-GLUCOSE | metformin | ENDOPLASMIC-RETICULUM STRESS | DILATED CARDIOMYOPATHY | CONSCIOUS DOGS | NITRIC-OXIDE PRODUCTION | MYOCARDIAL FATTY-ACID | IN-VIVO | PERIPHERAL VASCULAR DISEASE | INDUCED CARDIAC-HYPERTROPHY | GLUCOSE-UPTAKE | HEMATOLOGY | Metformin - therapeutic use | Rats, Wistar | Apoptosis - drug effects | Heart Failure - enzymology | Nitric Oxide Synthase Type III - biosynthesis | Natriuretic Peptides - biosynthesis | Aminoimidazole Carboxamide - pharmacology | Cardiotonic Agents - therapeutic use | Myocytes, Cardiac - enzymology | Ribonucleotides - pharmacology | Protein Processing, Post-Translational - drug effects | Ventricular Dysfunction, Left - genetics | Ultrasonography | Ventricular Dysfunction, Left - enzymology | Heart Failure - diagnostic imaging | Phosphorylation - drug effects | Drug Evaluation, Preclinical | Transforming Growth Factor beta1 - biosynthesis | Natriuretic Peptides - genetics | Pyrazoles - pharmacology | Nitric Oxide - biosynthesis | Cells, Cultured - drug effects | AMP-Activated Protein Kinases - antagonists & inhibitors | Insulin Resistance | Rats | Transforming Growth Factor beta1 - genetics | Pyrimidines - pharmacology | Nitric Oxide Synthase Type III - genetics | Cells, Cultured - enzymology | Disease Progression | Ventricular Dysfunction, Left - diagnostic imaging | Heart Failure - drug therapy | Gene Expression Regulation - drug effects | AMP-Activated Protein Kinases - physiology | Animals | Myocytes, Cardiac - drug effects | Ventricular Dysfunction, Left - drug therapy | Aminoimidazole Carboxamide - analogs & derivatives | Dogs | Fibrosis | Oxidative Stress - drug effects | Prevention | Oxidative stress | Usage | Demographic aspects | Animal models in research | Physiological aspects | Dosage and administration | Cyclic adenylic acid | Research | Protein kinases | Index Medicus | Abridged Index Medicus
Journal Article
International Journal of Cardiology, ISSN 0167-5273, 2015, Volume 185, pp. 198 - 208
Journal Article
Cardiovascular Research, ISSN 0008-6363, 06/2015, Volume 106, Issue 3, pp. 421 - 431
Journal Article