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Journal Article
Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 07/2014, Volume 34, Issue 7, pp. 1446 - 1458
OBJECTIVE—Pulmonary vascular remodeling, the pathological hallmark of pulmonary arterial hypertension, is attributed to proliferation, apoptosis resistance,... 
anoxia | muscle | pulmonary | protein-lysine 6-oxidase | hypertension | extracellular matrix | smooth | COLLAGEN | muscle, smooth | AORTIC-ANEURYSMS | RAT | BONE MORPHOGENETIC PROTEIN | hypertension, pulmonary | PROLIFERATION | HYPOXIA | CROSS-TALK | GROWTH-FACTORS | ELASTIN | PERIPHERAL VASCULAR DISEASE | SMOOTH-MUSCLE-CELLS | HEMATOLOGY | Antihypertensive Agents - pharmacology | Fibroblasts - enzymology | Humans | Middle Aged | Monocrotaline | Myocytes, Smooth Muscle - pathology | Male | Hypertrophy, Right Ventricular - etiology | RNA, Messenger - metabolism | Ventricular Dysfunction, Right - enzymology | Case-Control Studies | Cell Hypoxia | Young Adult | Aged, 80 and over | Adult | Female | Ventricular Dysfunction, Right - physiopathology | Hypertension, Pulmonary - drug therapy | Hypertension, Pulmonary - enzymology | Disease Models, Animal | Elastin - metabolism | Isoenzymes | Myocytes, Smooth Muscle - enzymology | Cells, Cultured | Enzyme Inhibitors - pharmacology | Rats | Familial Primary Pulmonary Hypertension | Hypertension, Pulmonary - genetics | Hypoxia - complications | Pulmonary Artery - drug effects | Fibroblasts - pathology | Hypertrophy, Right Ventricular - enzymology | Pulmonary Artery - enzymology | Gene Expression Regulation, Enzymologic | Ventricular Dysfunction, Right - prevention & control | Collagen - metabolism | Protein-Lysine 6-Oxidase - antagonists & inhibitors | Muscle, Smooth, Vascular - pathology | Animals | Ventricular Dysfunction, Right - etiology | Protein-Lysine 6-Oxidase - metabolism | Hypertrophy, Right Ventricular - prevention & control | Mice | Protein-Lysine 6-Oxidase - genetics | Hypertension, Pulmonary - etiology | Hypertension, Pulmonary - pathology | Muscle, Smooth, Vascular - enzymology | Pulmonary Artery - pathology
Journal Article
PEDIATRIC RESEARCH, ISSN 0031-3998, 12/2015, Volume 78, Issue 6, pp. 634 - 640
BACKGROUND: Pulmonary hypertension (PH) worsens clinical outcomes in former preterm infants with bronchopulmonary dysplasia (BPD). Oxidant stress disrupts... 
OVEREXPRESSION | VEGF | INFANTS | NITRIC-OXIDE | PEDIATRICS | MICE | HYPEROXIA | EXTRACELLULAR-SUPEROXIDE DISMUTASE | RAT LUNG | ENDOTHELIAL GROWTH-FACTOR | LUNG STRUCTURE | Bronchopulmonary Dysplasia - enzymology | Phosphorylation | Superoxide Dismutase - genetics | Vascular Remodeling | Oxidative Stress | Ventricular Dysfunction, Right - genetics | Bronchopulmonary Dysplasia - pathology | Hypertension, Pulmonary - physiopathology | Bronchopulmonary Dysplasia - physiopathology | Vascular Endothelial Growth Factor A - metabolism | Ventricular Dysfunction, Right - enzymology | Hypertension, Pulmonary - chemically induced | Pulmonary Alveoli - enzymology | Bronchopulmonary Dysplasia - genetics | Hypertrophy, Right Ventricular - physiopathology | Bleomycin | Ventricular Dysfunction, Right - physiopathology | Nitric Oxide Synthase Type III - metabolism | Ventricular Dysfunction, Right - chemically induced | Hypertension, Pulmonary - enzymology | Hypertrophy, Right Ventricular - genetics | Pulmonary Alveoli - blood supply | Animals, Newborn | Genetic Predisposition to Disease | Pulmonary Alveoli - pathology | Signal Transduction | Mice, Inbred C57BL | Vascular Endothelial Growth Factor Receptor-2 - metabolism | Hypertension, Pulmonary - genetics | Superoxide Dismutase - deficiency | Pulmonary Artery - physiopathology | Hypertrophy, Right Ventricular - enzymology | Pulmonary Artery - enzymology | Mice, Knockout | Phenotype | Animals | Bronchopulmonary Dysplasia - chemically induced | Hypertrophy, Right Ventricular - chemically induced | Ventricular Pressure | Endothelial Cells - pathology | Nitric Oxide - metabolism | Endothelial Cells - enzymology | Hypertension, Pulmonary - pathology | Pulmonary Artery - pathology | Ventricular Function, Right
Journal Article
American Journal of Physiology - Heart and Circulatory Physiology, ISSN 0363-6135, 05/2013, Volume 305, Issue 4, pp. H551 - H562
Alterations in the ubiquitin-proteasome system (UPS) have been described in left ventricular hypertrophy and failure, although results have been inconsistent.... 
Heart failure | Ubiquitin | Cardiac hypertrophy | Right ventricle | Proteasome | SYSTEM | proteasome | heart failure | PRESSURE-OVERLOAD | CARDIAC & CARDIOVASCULAR SYSTEMS | PHYSIOLOGY | TGF-BETA | HEART-FAILURE | MYOCARDIAL-ISCHEMIA | DILATED CARDIOMYOPATHY | 26S PROTEASOME | ubiquitin | MURINE MODEL | right ventricle | PERIPHERAL VASCULAR DISEASE | INDUCED CARDIAC-HYPERTROPHY | cardiac hypertrophy | UP-REGULATION | Genetic Therapy | Apoptosis - drug effects | Ventricular Dysfunction, Right - genetics | Heart Failure - enzymology | Heart Failure - physiopathology | Ubiquitin - metabolism | Male | Hypertrophy, Right Ventricular - etiology | Pulmonary Artery - surgery | Ventricular Dysfunction, Right - enzymology | Heart Failure - prevention & control | Hypertrophy, Right Ventricular - physiopathology | Time Factors | Hypertrophy, Right Ventricular - pathology | Ventricular Dysfunction, Right - physiopathology | Ventricular Function, Right - drug effects | Heart Failure - etiology | Hypertrophy, Right Ventricular - genetics | Disease Models, Animal | Constriction | Proteasome Inhibitors - pharmacology | Gene Expression Regulation | Heart Failure - genetics | Mice, Transgenic | Pulmonary Artery - physiopathology | Heart Failure - pathology | Hypertrophy, Right Ventricular - enzymology | Proteasome Endopeptidase Complex - genetics | Ventricular Dysfunction, Right - prevention & control | Myocardium - enzymology | Animals | Signal Transduction - drug effects | Ventricular Dysfunction, Right - etiology | Hypertrophy, Right Ventricular - prevention & control | Hemodynamics - drug effects | Mice | Proteasome Endopeptidase Complex - metabolism | Ventricular Dysfunction, Right - pathology | Heart enlargement | Physiological aspects | Cellular signal transduction | Research | Ubiquitin-proteasome system | Health aspects | Integrative Cardiovascular Physiology and Pathophysiology
Journal Article
Respiratory Research, ISSN 1465-9921, 08/2016, Volume 17, Issue 1, p. 108
Background: Pulmonary arterial hypertension (PAH) is associated with inflammatory response but it is unknown whether it is associated with alterations in NNMT... 
Idiopathic pulmonary hypertension | Isolated lungs | Monocrotaline | Prostacyclin | Pulmonary endothelial dysfunction | Pulmonary hypertension | Nicotinamide N-methyltransferase | PYRROLE-TREATED RATS | ENDOTHELIAL DYSFUNCTION | DILATED CARDIOMYOPATHY | 1-METHYLNICOTINAMIDE MNA | CONCANAVALIN-A | RESPIRATORY SYSTEM | ARTERIAL-HYPERTENSION | LIVER | NITRIC-OXIDE | PERFUSED LUNGS | Niacinamide - analogs & derivatives | Epoprostenol - metabolism | Liver - enzymology | Rats, Wistar | Humans | Middle Aged | Hypertension, Pulmonary - physiopathology | Male | Hypertrophy, Right Ventricular - etiology | Nicotinamide N-Methyltransferase - metabolism | Ventricular Dysfunction, Right - enzymology | Hypertension, Pulmonary - chemically induced | Case-Control Studies | Lung - enzymology | Hypertrophy, Right Ventricular - physiopathology | Time Factors | Adult | Female | Ventricular Dysfunction, Right - physiopathology | Hypertension, Pulmonary - enzymology | Disease Models, Animal | Lung - pathology | Niacinamide - blood | Niacinamide - metabolism | Signal Transduction | Hypertrophy, Right Ventricular - enzymology | Disease Progression | Endothelin-1 - blood | Animals | Ventricular Dysfunction, Right - etiology | Nitric Oxide - metabolism | Hypertension, Pulmonary - pathology | 6-Ketoprostaglandin F1 alpha - blood | Ventricular Function, Right | Research | Prostacyclin, Pulmonary endothelial dysfunction
Journal Article
American Journal of Physiology - Heart and Circulatory Physiology, ISSN 0363-6135, 12/2010, Volume 299, Issue 6, pp. H1854 - H1864
Xu EZ, Kantores C, Ivanovska J, Engelberts D, Kavanagh BP, McNamara PJ, Jankov RP. Rescue treatment with a Rho-kinase inhibitor normalizes right ventricular... 
Hypoxia | Smooth muscle cells | Endothelin-1 | Apoptosis | MEDIATED VASOCONSTRICTION | hypoxia | LUNG | CARDIAC & CARDIOVASCULAR SYSTEMS | PHYSIOLOGY | G-PROTEINS | apoptosis | NEONATAL-RATS | smooth muscle cells | NEWBORN RAT | NONMUSCLE MYOSIN-II | CHRONIC HYPOXIA | ARTERIAL SMOOTH-MUSCLE | NITRIC-OXIDE | PERIPHERAL VASCULAR DISEASE | endothelin-1 | Apoptosis - drug effects | Hypertension, Pulmonary - physiopathology | Hypertrophy, Right Ventricular - etiology | Hypertrophy, Right Ventricular - physiopathology | RNA Interference | rho-Associated Kinases - metabolism | Injections, Subcutaneous | Aging | Ventricular Dysfunction, Right - physiopathology | Hypertension, Pulmonary - drug therapy | Hypertension, Pulmonary - enzymology | Disease Models, Animal | Muscle, Smooth, Vascular - drug effects | Amides - pharmacology | Hypoxia - enzymology | Pyridines - administration & dosage | Rats | Ventricular Dysfunction, Right - drug therapy | Hypoxia - complications | Pulmonary Artery - drug effects | Pulmonary Artery - enzymology | Protein Kinase Inhibitors - administration & dosage | Ventricular Dysfunction, Right - etiology | Hypertrophy, Right Ventricular - prevention & control | Hypoxia - physiopathology | Receptor, Endothelin A - metabolism | Hemodynamics | Chronic Disease | Hypertension, Pulmonary - etiology | Muscle, Smooth, Vascular - enzymology | Age Factors | 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - analogs & derivatives | Ventricular Dysfunction, Right - enzymology | rho-Associated Kinases - antagonists & inhibitors | Endothelin-1 - metabolism | Cells, Cultured | rho-Associated Kinases - genetics | Myocardium - pathology | Hypertrophy, Right Ventricular - enzymology | Muscle, Smooth, Vascular - pathology | Myocardium - enzymology | Animals | 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - pharmacology | Cell Proliferation - drug effects | Protein Kinase Inhibitors - pharmacology | Pyridines - pharmacology | Amides - administration & dosage | Ventricular Remodeling - drug effects | Pulmonary Artery - pathology | Ventricular Function, Right | Complications and side effects | Care and treatment | Enzyme inhibitors | Research | Health aspects | Pulmonary hypertension | Heart ventricle, Right
Journal Article
American Journal of Respiratory Cell and Molecular Biology, ISSN 1044-1549, 06/2015, Volume 52, Issue 6, pp. 717 - 727
Chronic neonatal pulmonary hypertension frequently culminates in right ventricular (RV) failure and death. In juvenile rats, RV systolic dysfunction secondary... 
Echocardiography | Y-27632 | Fasudil | Phosphodiesterase | PRESSURE-OVERLOAD | SILDENAFIL | MYOCARDIAL-INFARCTION | fasudil | PHOSPHODIESTERASE-5 EXPRESSION | BIOCHEMISTRY & MOLECULAR BIOLOGY | echocardiography | CELL BIOLOGY | CRUCIAL ROLE | HYPERTROPHY | INHIBITION | RESPIRATORY SYSTEM | ARTERIAL-HYPERTENSION | phosphodiesterase | RIGHT-HEART-FAILURE | MOLECULAR-MECHANISMS | rho-Associated Kinases - physiology | Purines - pharmacology | 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - analogs & derivatives | Rats | Ventricular Dysfunction, Right - drug therapy | rhoA GTP-Binding Protein - metabolism | Hypertrophy, Right Ventricular - etiology | Hypertrophy, Right Ventricular - enzymology | Sulfonamides - pharmacology | Ventricular Dysfunction, Right - enzymology | 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - administration & dosage | Piperazines - pharmacology | rho-Associated Kinases - antagonists & inhibitors | Hypertrophy, Right Ventricular - drug therapy | Sildenafil Citrate | Animals | Heart Ventricles - enzymology | Ventricular Dysfunction, Right - etiology | Vascular Resistance - drug effects | Hypertension, Pulmonary - drug therapy | Cyclic Nucleotide Phosphodiesterases, Type 5 - metabolism | Hypertension, Pulmonary - enzymology | Hypertension, Pulmonary - complications | Heart failure | Heart | Kinases | Molecular biology | Rodents | Pulmonary hypertension
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
Journal Article
American Journal of Respiratory Cell and Molecular Biology, ISSN 1044-1549, 05/2018, Volume 58, Issue 5, pp. 636 - 647
Sickle cell disease (SCD) is associated with intravascular hemolysis and oxidative inhibition of nitric oxide (NO) signaling. BAY 54-6544 is a small-molecule... 
Sickle cell disease | Pulmonary hypertension | Soluble guanylate cyclase | HEMOGLOBIN | REDOX STATE | PULMONARY ARTERIAL-HYPERTENSION | pulmonary hypertension | BIOCHEMISTRY & MOLECULAR BIOLOGY | HEART-FAILURE | CINACIGUAT | soluble guanylate cyclase | BLOOD-PRESSURE | sickle cell disease | CELL BIOLOGY | MEDIATED VASODILATION | CYCLIC-GMP | HEME | TRANSGENIC-KNOCKOUT MICE | RESPIRATORY SYSTEM | Enzyme Activators - pharmacology | Hypertrophy, Left Ventricular - enzymology | Soluble Guanylyl Cyclase - metabolism | Ventricular Dysfunction, Right - genetics | Hypertension, Pulmonary - physiopathology | Ventricular Dysfunction, Right - enzymology | Hypertrophy, Left Ventricular - genetics | Heart Ventricles - enzymology | Arterial Pressure - drug effects | Ventricular Dysfunction, Right - physiopathology | Hypertension, Pulmonary - drug therapy | Ventricular Function, Right - drug effects | Hypertension, Pulmonary - enzymology | Disease Models, Animal | Sildenafil Citrate - pharmacology | Anemia, Sickle Cell - complications | Hypertrophy, Left Ventricular - prevention & control | Ventricular Pressure - drug effects | Morpholines - pharmacology | Hypertension, Pulmonary - genetics | Mice, Transgenic | Ventricular Dysfunction, Right - drug therapy | Pulmonary Artery - physiopathology | Pulmonary Artery - drug effects | Pyrimidines - pharmacology | Pulmonary Artery - enzymology | Animals | Heart Ventricles - physiopathology | Enzyme Activation | Hypertrophy, Left Ventricular - physiopathology | Vasodilation - drug effects | Nitric Oxide - metabolism | Enzyme Activators - pharmacokinetics | Ventricular Remodeling - drug effects | Anemia, Sickle Cell - genetics | Heart Ventricles - drug effects | Homeostasis | Smooth muscle | Kinases | Guanylate cyclase | Tibia | Rodents | Cyclic GMP | Heme | Blood pressure | Heart diseases | Heart failure | Enzymes | Catheterization | Anemia | Pulmonary arteries | Transgenic mice | Bioavailability | FDA approval | Pulmonary artery | Endothelium | Studies | Sodium | Nitric oxide | Acetylcholine | Intubation | Sildenafil | Ventricle | Hypertrophy | Veins & arteries
Journal Article
Molecular and Cellular Biochemistry, ISSN 0300-8177, 1/2013, Volume 373, Issue 1, pp. 161 - 170
We assessed the time courses of mitochondrial biogenesis factors and respiration in the right ventricle (RV), gastrocnemius (GAS), and left ventricle (LV) in a... 
Life Sciences | Biochemistry, general | Mitochondria | Monocrotaline | Medical Biochemistry | Oncology | Right ventricular failure | PGC-1α | Cardiology | Pulmonary hypertension | PGC-1 alpha | PGC-1-ALPHA | RATS | 1ST 10 DECADES | EXERCISE | CELL BIOLOGY | OXIDATIVE CAPACITY | HYPERTROPHY | NEUROHUMORAL ACTIVATION | METABOLISM | HEART-FAILURE PATIENTS | AGE-RELATED-CHANGES | Sirtuin 1 - metabolism | RNA-Binding Proteins - genetics | Rats, Wistar | Heart Failure - enzymology | Mitochondria, Muscle - metabolism | Heart Failure - physiopathology | Hypertension, Pulmonary - physiopathology | Male | Ventricular Dysfunction, Right - enzymology | Hypertension, Pulmonary - chemically induced | Nuclear Respiratory Factor 1 - genetics | Sirtuin 1 - genetics | Heart Ventricles - enzymology | Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha | Nuclear Respiratory Factor 1 - metabolism | Ventricular Dysfunction, Right - physiopathology | Citrate (si)-Synthase - metabolism | Heart Failure - etiology | Hypertension, Pulmonary - enzymology | Gene Expression | Oxygen Consumption | Rats | Transcription Factors - genetics | Transcription Factors - metabolism | Animals | Heart Ventricles - physiopathology | Ventricular Dysfunction, Right - etiology | Citrate (si)-Synthase - genetics | Muscle, Skeletal - pathology | RNA-Binding Proteins - metabolism | Hypertension, Pulmonary - complications | Hypertension | Cardiovascular disease | Biosynthesis | Gene expression
Journal Article
The International Journal of Cardiovascular Imaging, ISSN 1569-5794, 4/2015, Volume 31, Issue 4, pp. 669 - 679
Consistent protocols for the assessment of diastolic and systolic cardiac function to assure the comparability of existing data on preclinical models are... 
Heart failure | Echocardiography | Medicine & Public Health | Magnetic resonance imaging | Cardiac disease | Electrocardiography | Cardiology | Doppler | INBRED MOUSE STRAINS | CARDIAC & CARDIOVASCULAR SYSTEMS | MRI | HEART-FAILURE | MODEL | ECHOCARDIOGRAPHIC-ASSESSMENT | CARDIAC-HYPERTROPHY | IN-VIVO | RADIOLOGY, NUCLEAR MEDICINE & MEDICAL IMAGING | Predictive Value of Tests | Hypertrophy, Left Ventricular - enzymology | Ventricular Function, Left | Ventricular Dysfunction, Right - genetics | Heart Failure - enzymology | Heart Failure - physiopathology | Hypertrophy, Left Ventricular - diagnosis | Myosin Heavy Chains - genetics | Male | Cardiomyopathy, Hypertrophic - enzymology | Ventricular Dysfunction, Right - enzymology | Hypertrophy, Right Ventricular - physiopathology | Ventricular Remodeling | Calcineurin - genetics | Hypertrophy, Left Ventricular - genetics | Ventricular Dysfunction, Left - genetics | Echocardiography, Doppler | Ventricular Dysfunction, Left - enzymology | Female | Ventricular Dysfunction, Right - physiopathology | Heart Failure - diagnosis | Hypertrophy, Right Ventricular - genetics | Disease Models, Animal | High-Throughput Screening Assays - methods | Promoter Regions, Genetic | Cardiomyopathy, Hypertrophic - genetics | Genetic Predisposition to Disease | Hypertrophy, Right Ventricular - diagnosis | Mice, Inbred C57BL | Heart Failure - genetics | Mice, Transgenic | Ventricular Dysfunction, Left - diagnosis | Hypertrophy, Right Ventricular - enzymology | Ventricular Dysfunction, Right - diagnosis | Cardiomyopathy, Hypertrophic - diagnosis | Disease Progression | Ventricular Dysfunction, Left - physiopathology | Magnetic Resonance Imaging | Phenotype | Animals | Cardiomyopathy, Hypertrophic - physiopathology | Hemodynamics | Hypertrophy, Left Ventricular - physiopathology | Calcineurin - metabolism | Ventricular Function, Right | Ventricular Myosins - genetics | Heart | Genetic engineering | Electrocardiogram
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
Journal Article
Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 06/2017, Volume 37, Issue 6, pp. 1138 - 1146
Objective-Oxidative stress and inflammation play key roles in the development of pulmonary arterial hypertension (PAH). Cyclophilin A (CypA) is secreted in... 
acetylation | hypertension, pulmonary | cyclophilin A | endothelial cell | oxidative stress | ACTIVATION | hypertension pulmonary | MOUSE | MUSCLE-CELL PROLIFERATION | BINDING-PROTEIN | CYCLOSPORINE-A | ARTERIAL-HYPERTENSION | GROWTH | DISEASE | PROMOTING INFLAMMATION | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | Inflammation - pathology | Phosphorylation | Muscle, Smooth, Vascular - metabolism | Apoptosis - drug effects | Ventricular Dysfunction, Right - genetics | Humans | Caspase 3 - metabolism | Myocytes, Smooth Muscle - pathology | Hypertension, Pulmonary - physiopathology | NF-kappa B - metabolism | Ventricular Dysfunction, Right - enzymology | Cyclosporins - pharmacology | Muscle, Smooth, Vascular - physiopathology | Inflammation Mediators - metabolism | Ventricular Dysfunction, Right - physiopathology | Cyclophilin A - genetics | Acetylation | Myocytes, Smooth Muscle - metabolism | Hypertension, Pulmonary - enzymology | Cyclophilin A - metabolism | Genetic Predisposition to Disease | Oxidation-Reduction | Signal Transduction | Mice, Inbred C57BL | Cells, Cultured | Enzyme Inhibitors - pharmacology | Hypertension, Pulmonary - genetics | Mice, Transgenic | Cell Adhesion Molecules - metabolism | Cyclophilin A - antagonists & inhibitors | Muscle, Smooth, Vascular - pathology | Phenotype | Animals | Inflammation - genetics | Ventricular Pressure | Oxidative Stress - drug effects | Endothelial Cells - pathology | Endothelial Cells - enzymology | Hypertension, Pulmonary - pathology | Inflammation - enzymology | Ventricular Function, Right | Endothelial Cells - drug effects | Inflammation - physiopathology | inflammation | pulmonary arterial hypertension
Journal Article