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Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 11/2012, Volume 32, Issue 11, pp. 2580 - 2588
OBJECTIVE—Vascular calcification significantly increases cardiovascular morbidity and mortality. We recently reported that the deficiency of cartilage... 
Smooth muscle cell | Calcification | Animal model of human disease remodeling | MicroRNA | Protease | animal model of human disease remodeling | CELLS | smooth muscle cell | PATHOBIOLOGY | MECHANISMS | OLIGOMERIC MATRIX PROTEIN | protease | PHOSPHATE | IN-VITRO | ROLES | ARTERIAL CALCIFICATION | ANEURYSM DEVELOPMENT | microRNA | PERIPHERAL VASCULAR DISEASE | calcification | CHRONIC KIDNEY-DISEASE | HEMATOLOGY | Up-Regulation | Carotid Artery Diseases - chemically induced | Humans | MicroRNAs - metabolism | Matrilin Proteins | Nephrectomy | RNA Interference | Time Factors | Carotid Artery Diseases - pathology | Transcription, Genetic | 3' Untranslated Regions | Real-Time Polymerase Chain Reaction | Organ Culture Techniques | Disease Models, Animal | Uremia - enzymology | Myocytes, Smooth Muscle - enzymology | Down-Regulation | Computational Biology | Rats | Vascular Calcification - pathology | Rats, Sprague-Dawley | Kidney Failure, Chronic - genetics | ADAM Proteins - metabolism | Aortic Diseases - genetics | Carotid Artery Diseases - enzymology | Carotid Artery, Common - enzymology | Carotid Artery Diseases - genetics | Kidney Failure, Chronic - complications | ADAMTS7 Protein | Carotid Artery, Common - pathology | ADAM Proteins - genetics | Muscle, Smooth, Vascular - enzymology | Vascular Calcification - genetics | Glycoproteins - metabolism | Myocytes, Smooth Muscle - pathology | Aortic Diseases - chemically induced | Transfection | Uremia - pathology | Female | Vascular Calcification - enzymology | Aortic Diseases - enzymology | Aorta, Abdominal - pathology | Kidney Failure, Chronic - enzymology | Extracellular Matrix Proteins - metabolism | Aortic Diseases - pathology | Promoter Regions, Genetic | Calcium Chloride | Cartilage Oligomeric Matrix Protein | Cells, Cultured | Aorta, Abdominal - enzymology | Gene Expression Regulation, Enzymologic | Muscle, Smooth, Vascular - pathology | Animals | Vascular Calcification - chemically induced
Journal Article
Circulation Research, ISSN 0009-7330, 09/2013, Volume 113, Issue 8, pp. 1013 - 1022
RATIONALE:Blood–brain–barrier (BBB) breakdown and cerebral edema result from postischemic inflammation and contribute to mortality and morbidity after ischemic... 
Vascular system injuries | Animal model of human disease remodeling | Inflammation | Ischemic stroke | Neutrophils | animal model of human disease remodeling | MIDDLE CEREBRAL-ARTERY | CARDIAC & CARDIOVASCULAR SYSTEMS | RAT | VESSEL MATURATION | SELECTIN-DEFICIENT MICE | HEMORRHAGIC TRANSFORMATION | MATRIX METALLOPROTEINASES | CEACAM1 | vascular system injuries | inflammation | GELATINASE-B | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | neutrophils | EXPRESSION | ischemic stroke | OCCLUSION | Infarction, Middle Cerebral Artery - physiopathology | Infarction, Middle Cerebral Artery - prevention & control | Capillary Permeability | Humans | Carcinoembryonic Antigen - genetics | Male | Infarction, Middle Cerebral Artery - immunology | Motor Activity | Neutrophil Infiltration | Sulfones - pharmacology | Antigens, CD - metabolism | Brain Edema - enzymology | Carcinoembryonic Antigen - metabolism | Atrophy | Behavior, Animal | Matrix Metalloproteinase 9 - metabolism | Flow Cytometry | Time Factors | Heterocyclic Compounds, 1-Ring - pharmacology | Infarction, Middle Cerebral Artery - genetics | Inflammation Mediators - metabolism | Brain Edema - immunology | Disease Models, Animal | Neutrophils - pathology | Blood-Brain Barrier - immunology | Neutrophil Activation | Neutrophils - enzymology | Brain Edema - pathology | Mice, Inbred C57BL | Neutrophils - drug effects | Neutrophils - immunology | Infarction, Middle Cerebral Artery - pathology | Blood-Brain Barrier - drug effects | Cell Adhesion Molecules - metabolism | Mice, Knockout | Blood-Brain Barrier - pathology | Magnetic Resonance Imaging | Matrix Metalloproteinase Inhibitors - pharmacology | Animals | Blood-Brain Barrier - enzymology | Neurologic Examination | Mice | Infarction, Middle Cerebral Artery - enzymology | Microscopy, Fluorescence
Journal Article
Journal of the American Heart Association, ISSN 2047-9980, 11/2018, Volume 7, Issue 21, p. e009514
Journal Article
Cardiovascular Research, ISSN 0008-6363, 10/2018, Volume 114, Issue 12, pp. 1680 - 1690
Abstract Aims Generation of reproducible cardiac disease phenotypes in mice is instrumental for investigating mechanisms leading to heart failure (HF). For... 
Animal model of human disease remodelling | PRESSURE-OVERLOAD | ACTIVATION | CARDIAC & CARDIOVASCULAR SYSTEMS | STENOSIS | HEART-FAILURE | Cardiac remodelling | LEFT-VENTRICULAR HYPERTROPHY | REPRODUCIBILITY | MURINE MODEL | Experimental heart failure | Fibrosis | MOUSE MODEL | GENE-EXPRESSION | Hypertrophy
Journal Article
Circulation Research, ISSN 0009-7330, 02/2013, Volume 112, Issue 3, pp. 432 - 440
RATIONALE:Human genetics have implicated the 5-lipoxygenase enzyme in the pathogenesis of cardiovascular disease, and an inhibitor of the 5-lipoxygenase... 
animal model of human disease remodeling | vascular injury | restenosis | smooth muscle cell | inflammation | angioplasty and stenting | leukotrienes | ARTERIAL INJURY | CARDIAC & CARDIOVASCULAR SYSTEMS | MYOCARDIAL-INFARCTION | NEOINTIMAL HYPERPLASIA | INTIMAL HYPERPLASIA | BALLOON ANGIOPLASTY | PERIPHERAL VASCULAR DISEASE | SMOOTH-MUSCLE-CELLS | EXTRACELLULAR-MATRIX | HEMATOLOGY | PROMOTES ATHEROSCLEROSIS | LEUKOTRIENE MODIFIERS | TENASCIN-C | Myeloid Cells - enzymology | Femoral Artery - pathology | Cell Proliferation | Vascular System Injuries - immunology | 5-Lipoxygenase-Activating Proteins - metabolism | Vascular System Injuries - genetics | Hyperplasia | Myocytes, Smooth Muscle - pathology | Muscle, Smooth, Vascular - immunology | Vascular System Injuries - enzymology | Male | Tenascin - metabolism | 5-Lipoxygenase-Activating Proteins - deficiency | Femoral Artery - enzymology | Vascular System Injuries - pathology | Femoral Artery - injuries | Neointima | Time Factors | Myeloid Cells - immunology | Bone Marrow Transplantation | Inflammation Mediators - metabolism | Leukotriene B4 - metabolism | Cysteine - metabolism | 5-Lipoxygenase-Activating Proteins - genetics | Disease Models, Animal | Endothelial Cells - metabolism | Myocytes, Smooth Muscle - enzymology | Mice, Inbred C57BL | Cells, Cultured | Genotype | Vascular System Injuries - prevention & control | Mice, Knockout | Leukotrienes - metabolism | Muscle, Smooth, Vascular - injuries | Muscle, Smooth, Vascular - pathology | Phenotype | Animals | Myocytes, Smooth Muscle - immunology | Myeloid Cells - transplantation | Mice | Endothelial Cells - pathology | Vascular Cell Adhesion Molecule-1 - metabolism | Muscle, Smooth, Vascular - enzymology | Cell Movement | Restenosis
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 2000, Volume 106, Issue 6, pp. 733 - 738
Journal Article
Journal of the American Heart Association, ISSN 2047-9980, 03/2015, Volume 4, Issue 3, p. e001733
Background-Atrial fibrillation (AF) is a complex disease process, and the molecular mechanisms underlying initiation and progression of the disease are... 
pathogenesis | atrial fibrillation | animal models of human disease remodeling | atrium | inflammation | CARDIAC & CARDIOVASCULAR SYSTEMS | RISK-FACTORS | SINUS | PROGNOSIS | HEART-FAILURE | PREVENTION | PREVALENCE | PATHOPHYSIOLOGY | ANIMAL-MODELS | DYSFUNCTION | Atrioventricular Block - genetics | Atrial Flutter - enzymology | Protein-Serine-Threonine Kinases - deficiency | AMP-Activated Protein Kinases - metabolism | Reactive Oxygen Species - metabolism | Age Factors | Ventricular Function, Left | Heart Failure - enzymology | Humans | Heart Failure - physiopathology | Male | Atrial Fibrillation - enzymology | Atrial Fibrillation - physiopathology | Cardiomyopathies - enzymology | Necrosis | Myocytes, Cardiac - enzymology | Cardiomyopathies - genetics | Cardiomyopathies - physiopathology | Ventricular Dysfunction, Left - genetics | Ventricular Dysfunction, Left - enzymology | Atrioventricular Block - enzymology | Atrial Fibrillation - pathology | Heart Rate | Atrioventricular Block - physiopathology | Connexin 43 - metabolism | Mice, Inbred C57BL | Inflammation Mediators - blood | Protein-Serine-Threonine Kinases - genetics | Genotype | Heart Failure - genetics | Atrial Flutter - genetics | Atrial Fibrillation - genetics | Atrial Flutter - physiopathology | Disease Progression | Ventricular Dysfunction, Left - physiopathology | Connexins - metabolism | Mice, Knockout | Myocytes, Cardiac - pathology | Phenotype | Animals | Exercise Tolerance | Fibrosis | Apoptosis
Journal Article
Journal of Cardiovascular Translational Research, ISSN 1937-5387, 10/2013, Volume 6, Issue 5, pp. 852 - 860
The development of left ventricular hypertrophy and dysfunction in aortic regurgitation (AR) has only been sparsely studied experimentally. In a new model of... 
Human Genetics | Biomedical Engineering | Proteins | Medicine & Public Health | Aortic valve regurgitation | Animal models of human disease remodeling | Ventricular function | Cardiology | Medicine/Public Health, general | Biomedicine general | Hypertrophy | MEDICINE, RESEARCH & EXPERIMENTAL | PRESSURE-OVERLOAD | ACTIVATION | CARDIAC & CARDIOVASCULAR SYSTEMS | VOLUME OVERLOAD | HEART-FAILURE | CARDIOMYOPATHY | KINASE-II | PATHOLOGICAL CARDIAC-HYPERTROPHY | GROWTH | ADAPTATION | EXPRESSION | Phosphorylation | Ventricular Function, Left | JNK Mitogen-Activated Protein Kinases - metabolism | Male | Echocardiography, Doppler, Color | Extracellular Signal-Regulated MAP Kinases - metabolism | Time Factors | Myocardium - metabolism | p38 Mitogen-Activated Protein Kinases - metabolism | Proto-Oncogene Proteins c-akt - metabolism | Aortic Valve Insufficiency - complications | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism | Disease Models, Animal | Aortic Valve Insufficiency - metabolism | Aortic Valve Insufficiency - diagnostic imaging | Atrial Natriuretic Factor - metabolism | Signal Transduction | Hypertrophy, Left Ventricular - etiology | Hypertrophy, Left Ventricular - metabolism | Aortic Valve Insufficiency - physiopathology | Rats | Ventricular Dysfunction, Left - etiology | Myocardium - pathology | Rats, Sprague-Dawley | Ventricular Dysfunction, Left - diagnostic imaging | Ventricular Dysfunction, Left - physiopathology | Ventricular Dysfunction, Left - metabolism | Animals | Hypertrophy, Left Ventricular - physiopathology | Chronic Disease | Calcineurin - metabolism | Hypertrophy, Left Ventricular - diagnostic imaging | Physiological aspects | Analysis | Aortic valve insufficiency
Journal Article
Journal Article
Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 05/2017, Volume 37, Issue 8, pp. 1513 - 1523
OBJECTIVE—Pulmonary arterial hypertension (PAH) is a vascular disease not restricted to the lungs. Many signaling pathways described in PAH are also of... 
coronary artery disease | comorbidity | vascular remodeling | pulmonary hypertension | coronary remodeling | SELECTIVE-INHIBITION | CELLS | ACTIVATION | DNA-DAMAGE | JQ1 | PREVALENCE | BROMODOMAIN | HEART-DISEASE | ENDOTHELIUM | PERIPHERAL VASCULAR DISEASE | DYSFUNCTION | HEMATOLOGY | RNA, Small Interfering - genetics | Cell Proliferation | Muscle, Smooth, Vascular - metabolism | Epigenesis, Genetic | Humans | Myocytes, Smooth Muscle - pathology | Male | MicroRNAs - metabolism | Case-Control Studies | Coronary Vessels - metabolism | RNA Interference | Coronary Artery Disease - pathology | Inflammation Mediators - metabolism | Nuclear Proteins - genetics | Interleukin-6 - metabolism | Myocytes, Smooth Muscle - metabolism | Disease Models, Animal | Coronary Vessels - pathology | Genetic Predisposition to Disease | Interleukin-6 - genetics | Coronary Artery Disease - metabolism | Cells, Cultured | Hypertension, Pulmonary - genetics | Nuclear Proteins - metabolism | Poly (ADP-Ribose) Polymerase-1 - metabolism | Hypertension, Pulmonary - metabolism | Transcription Factors - genetics | Rats, Sprague-Dawley | Transcription Factors - metabolism | Muscle, Smooth, Vascular - pathology | Phenotype | Animals | Vascular Remodeling - genetics | Coronary Artery Disease - genetics | MicroRNAs - genetics | DNA Damage | Hypertension, Pulmonary - pathology | Poly (ADP-Ribose) Polymerase-1 - genetics | Apoptosis | RNA, Small Interfering - metabolism
Journal Article
The Journal of clinical investigation, ISSN 0021-9738, 01/2004, Volume 113, Issue 2, pp. 148 - 157
Journal Article
JOURNAL OF CLINICAL INVESTIGATION, ISSN 0021-9738, 01/2004, Volume 113, Issue 2, pp. 148 - 157
A set of lung diseases share the tendency for the development of progressive fibrosis ultimately leading to respiratory failure. This review examines the... 
MEDICINE, RESEARCH & EXPERIMENTAL | FAS LIGAND | GROWTH-FACTOR-BETA | TGF-BETA | ALVEOLAR EPITHELIAL-CELLS | GENE-EXPRESSION | IDIOPATHIC PULMONARY-FIBROSIS | PROTEASE-ACTIVATED RECEPTOR-1 | HERMANSKY-PUDLAK-SYNDROME | RESPIRATORY-DISTRESS-SYNDROME | BRONCHOALVEOLAR LAVAGE | Science in Medicine
Journal Article