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1981, ISBN 8716089936, Volume no. 112, 45
Book
Nature Medicine, ISSN 1078-8956, 07/2015, Volume 21, Issue 7, pp. 777 - 785
Journal Article
Circulation Research, ISSN 0009-7330, 10/2004, Volume 95, Issue 8, pp. 830 - 840
The pulmonary arteries (PA) in pulmonary arterial hypertension (PAH) are constricted and remodeled;. They have suppressed apoptosis, partly attributable to... 
Vascular remodeling | Smooth muscle | Proliferation | Apoptosis | ACTIVATION | CARDIAC & CARDIOVASCULAR SYSTEMS | proliferation | POTASSIUM CHANNELS | CARDIAC MYOCYTES | smooth muscle | RATS | apoptosis | RELAXATION | vascular remodeling | PERIPHERAL VASCULAR DISEASE | DIVERSITY | HEMATOLOGY | EXPRESSION | K+ CHANNELS | VASOCONSTRICTION | Apoptosis - drug effects | Myocytes, Smooth Muscle - pathology | Hypertrophy, Right Ventricular - etiology | Dichloroacetic Acid - therapeutic use | Hypertension, Pulmonary - chemically induced | Heart Failure - prevention & control | Oxidative Phosphorylation - drug effects | Potassium Channels, Voltage-Gated - metabolism | Vascular Resistance - drug effects | Hypertrophy, Right Ventricular - pathology | Hypertension, Pulmonary - drug therapy | Drug Evaluation, Preclinical | Myocytes, Smooth Muscle - drug effects | Heart Failure - etiology | Muscle, Smooth, Vascular - drug effects | Potassium Channels, Voltage-Gated - genetics | Cells, Cultured - drug effects | Rats | Monocrotaline - toxicity | Mitochondria - drug effects | Pulmonary Artery - drug effects | Organ Specificity | Shab Potassium Channels | Kv1.5 Potassium Channel | Cell Division - drug effects | Pulmonary Artery - cytology | Gene Expression Regulation - drug effects | Muscle, Smooth, Vascular - pathology | Animals | Dichloroacetic Acid - pharmacology | Hemodynamics - drug effects | Hypertension, Pulmonary - pathology | Hypertension, Pulmonary - complications | Index Medicus
Journal Article
Circulation: Heart Failure, ISSN 1941-3289, 05/2015, Volume 8, Issue 3, pp. 542 - 550
Background Pulmonary hypertension and right ventricular (RV) dysfunction are common in patients with advanced heart failure with preserved ejection fraction... 
heart failure, diastolic | hypertension, pulmonary | heart failure | ventricular function, right | pulmonary circulation | EUROPEAN-ASSOCIATION | CARDIAC & CARDIOVASCULAR SYSTEMS | ventricular function | GUIDELINES | pulmonary | PLANE SYSTOLIC EXCURSION | EXERCISE CAPACITY | right | diastolic | DISEASE | PHOSPHODIESTERASE-5 INHIBITION | ECHOCARDIOGRAPHY | DYSFUNCTION | hypertension | AMERICAN-SOCIETY | Predictive Value of Tests | Hypertension, Pulmonary - diagnosis | Prospective Studies | Humans | Middle Aged | Heart Failure - physiopathology | Hypertension, Pulmonary - physiopathology | Male | Arterial Pressure - drug effects | Adrenergic beta-1 Receptor Agonists - administration & dosage | Aged, 80 and over | Female | Ventricular Dysfunction, Right - physiopathology | Heart Failure - diagnosis | Hypertension, Pulmonary - drug therapy | Ventricular Function, Right - drug effects | Heart Failure - complications | Ventricular Function, Left - drug effects | Diagnostic Techniques, Cardiovascular | Infusions, Parenteral | Stroke Volume - drug effects | Ventricular Dysfunction, Right - drug therapy | Pulmonary Artery - physiopathology | Pulmonary Artery - drug effects | Ventricular Dysfunction, Right - diagnosis | Dobutamine - administration & dosage | Heart Failure - drug therapy | Ventricular Dysfunction, Right - etiology | Aged | Vasodilation - drug effects | Hypertension, Pulmonary - etiology | Index Medicus
Journal Article
FEBS Letters, ISSN 0014-5793, 01/2016, Volume 590, Issue 1, pp. 101 - 109
Pulmonary arterial hypertension ( PAH ) is characterized by excessive pulmonary arterial smooth muscle cells ( PASMC s) growth, partially in response to PDGF ‐... 
smooth muscle cells | Wnt signaling | vascular remodeling | pulmonary disease | PDGF | pulmonary hypertension | Proto-Oncogene Proteins c-sis - chemistry | Muscle, Smooth, Vascular - metabolism | Humans | Glycogen Synthase Kinase 3 beta | Wnt-5a Protein | Promoter Regions, Genetic - drug effects | Wnt Proteins - metabolism | Familial Primary Pulmonary Hypertension - metabolism | Pulmonary Artery - metabolism | Wnt Proteins - genetics | Protein Processing, Post-Translational - drug effects | RNA Interference | Phosphorylation - drug effects | Proto-Oncogene Proteins c-sis - pharmacology | Muscle, Smooth, Vascular - drug effects | Familial Primary Pulmonary Hypertension - pathology | Proto-Oncogene Proteins - metabolism | Recombinant Proteins - metabolism | Proto-Oncogene Proteins - antagonists & inhibitors | Proto-Oncogene Proteins c-sis - metabolism | beta Catenin - agonists | Cells, Cultured | Proto-Oncogene Proteins - genetics | Pulmonary Artery - drug effects | Recombinant Proteins - pharmacology | Glycogen Synthase Kinase 3 - metabolism | Muscle, Smooth, Vascular - cytology | beta Catenin - metabolism | beta Catenin - genetics | Pulmonary Artery - cytology | Gene Expression Regulation - drug effects | Muscle, Smooth, Vascular - pathology | Wnt Signaling Pathway - drug effects | beta Catenin - antagonists & inhibitors | Active Transport, Cell Nucleus - drug effects | Anticoagulants - pharmacology | Genes, Reporter - drug effects | Cell Proliferation - drug effects | Wnt Proteins - antagonists & inhibitors | Pulmonary Artery - pathology | Index Medicus
Journal Article
JACC (Journal of the American College of Cardiology), ISSN 0735-1097, 2015, Volume 65, Issue 7, pp. 668 - 680
Abstract Background Endothelial cell (EC) dysfunction plays a central role in the pathogenesis of pulmonary arterial hypertension (PAH), promoting... 
Cardiovascular | Internal Medicine | β-blocker | nebivolol | inflammation | endothelial dysfunction | pulmonary hypertension | CELLS | CARDIAC & CARDIOVASCULAR SYSTEMS | beta-blocker | RATS | CROSS-TALK | THERAPY | SMOOTH-MUSCLE HYPERPLASIA | ARTERIAL-HYPERTENSION | ANIMAL-MODELS | BLOCKADE | PROGRESSION | Ethanolamines - pharmacology | Benzopyrans - therapeutic use | Cell Proliferation | Rats, Wistar | Metoprolol - pharmacology | Humans | Monocrotaline | Adrenergic beta-1 Receptor Antagonists - pharmacology | Hypertension, Pulmonary - physiopathology | Endothelium, Vascular - drug effects | Male | Adrenergic beta-1 Receptor Antagonists - therapeutic use | Hypertension, Pulmonary - drug therapy | Cell Culture Techniques | Vascular Remodeling - drug effects | Benzopyrans - pharmacology | Disease Models, Animal | Nebivolol | Endothelium, Vascular - physiopathology | Rats | Metoprolol - therapeutic use | Pulmonary Artery - physiopathology | Pulmonary Artery - drug effects | Animals | Myocytes, Smooth Muscle | Cell Communication - drug effects | Endothelium, Vascular - pathology | Ethanolamines - therapeutic use | Hypertension, Pulmonary - pathology | Pulmonary Artery - pathology | Endothelial Cells - drug effects | Heart | Sects | Pulmonary hypertension | Endothelium | Studies | Cell growth | Pulmonary arteries | Mortality | Smooth muscle | Veins & arteries | Index Medicus | Abridged Index Medicus | Life Sciences
Journal Article
Nature Medicine, ISSN 1078-8956, 02/2016, Volume 22, Issue 2, pp. 154 - 162
Although the lung can undergo self-repair after injury, fibrosis in chronically injured or diseased lungs can occur at the expense of regeneration. Here we... 
MEDICINE, RESEARCH & EXPERIMENTAL | STEM-CELLS | ANGIOGENESIS | MACROPHAGE REGULATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | NOTCH | SIGNALING PROMOTES | CELL BIOLOGY | TO-MESENCHYMAL TRANSITION | ENDOTHELIAL-CELLS | DISEASE | SMOOTH-MUSCLE-CELLS | DIFFERENTIATION | Antibiotics, Antineoplastic - toxicity | Receptors, Notch - metabolism | Humans | Calcium-Binding Proteins - antagonists & inhibitors | Capillaries - drug effects | Hydrochloric Acid - toxicity | Smad3 Protein - metabolism | Pulmonary Circulation - physiology | Intercellular Signaling Peptides and Proteins - metabolism | Pulmonary Artery - metabolism | Receptors, CXCR - metabolism | Serrate-Jagged Proteins | Lung Injury - metabolism | Lung - metabolism | Membrane Proteins - metabolism | Pulmonary Fibrosis - metabolism | Capillaries - metabolism | Endothelial Cells - physiology | Wnt Signaling Pathway | Bleomycin - toxicity | Fibroblasts - metabolism | Jagged-1 Protein | Calcium-Binding Proteins - metabolism | Lung - pathology | Endothelial Cells - metabolism | RNA, Small Interfering - pharmacology | Vascular Endothelial Growth Factor Receptor-1 - metabolism | Pulmonary Artery - drug effects | Lung - physiology | Regeneration - physiology | Macrophages - metabolism | Regeneration - drug effects | Animals | Membrane Proteins - antagonists & inhibitors | Smad3 Protein - drug effects | Fibroblasts - drug effects | Lung - drug effects | Fibrosis | Fluorescent Antibody Technique | Macrophages - drug effects | Mice | Pulmonary Circulation - drug effects | Oligopeptides - pharmacology | Receptors, CXCR - agonists | Endothelial Cells - drug effects | Physiological aspects | Regeneration (Biology) | Lung diseases | Blood vessels | Angiogenesis | Pulmonary fibrosis | Cellular biology | Index Medicus
Journal Article
Journal of Thoracic and Cardiovascular Surgery, The, ISSN 0022-5223, 2013, Volume 146, Issue 3, pp. 522 - 529
Objectives Continuous flow in the Fontan circulation results in impairment of pulmonary artery endothelial function, increased pulmonary arterial resistance,... 
Cardiothoracic Surgery | NO | SVC | eNOS | nitric oxide | pulmonary artery | 50% of the maximal response | PVP | PVR | maximal response | pulmonary vein pressure | PA | endothelial nitric oxide synthase | superior vena cava | pulmonary vascular resistance | pulmonary artery pressure | EC | Emax | PAP | SURGERY | CARDIAC & CARDIOVASCULAR SYSTEMS | RABBIT LUNGS | RESPIRATORY SYSTEM | NITRIC-OXIDE SYNTHASE | VASCULAR-RESISTANCE | VASODILATION | RELEASE | BLOOD-FLOW | HYPERTENSION | EXPRESSION | BIDIRECTIONAL CAVOPULMONARY SHUNT | Hypertension, Pulmonary - physiopathology | Endothelium, Vascular - drug effects | Fontan Procedure - adverse effects | Pulmonary Artery - surgery | Endothelium, Vascular - surgery | Vasodilation | Dose-Response Relationship, Drug | Microcirculation | Pulmonary Artery - metabolism | Pulsatile Flow - drug effects | Time Factors | Swine | Models, Animal | Nitric Oxide Synthase Type III - metabolism | Vascular Resistance | Vasodilator Agents - pharmacology | Endothelium, Vascular - physiopathology | Pulmonary Artery - physiopathology | Pulmonary Artery - drug effects | Animals | Endothelium, Vascular - metabolism | Endothelium, Vascular - pathology | Pulmonary Circulation - drug effects | Hypertension, Pulmonary - etiology | Pulmonary Artery - pathology | Health aspects | Children | Endothelium | Index Medicus | Abridged Index Medicus
Journal Article
European Journal of Pharmacology, ISSN 0014-2999, 06/2017, Volume 804, pp. 111 - 116
Journal Article
Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 08/2014, Volume 34, Issue 8, pp. 1704 - 1715
OBJECTIVE—Pulmonary hypertension (PH) is a progressive disease arising from remodeling and narrowing of pulmonary arteries (PAs) resulting in high pulmonary... 
Adventitia | Fibroblast | NADPH oxidase | Pulmonary artery | pulmonary artery | ACTIVATION | adventitia | PROLIFERATION | FIBROBLASTS | NAD(P)H OXIDASE | fibroblast | CHRONIC HYPOXIA | MODELS | INFLAMMATION | NOX4 | PERIPHERAL VASCULAR DISEASE | SMOOTH-MUSCLE-CELLS | HEMATOLOGY | MOLECULAR-MECHANISMS | Up-Regulation | Antihypertensive Agents - pharmacology | Fibroblasts - enzymology | Cell Proliferation | Reactive Oxygen Species - metabolism | Humans | Monocrotaline | NADPH Oxidases - metabolism | Pyrroles | Extracellular Matrix - metabolism | Male | Dose-Response Relationship, Drug | Extracellular Matrix - genetics | Transfection | Time Factors | HEK293 Cells | Adventitia - enzymology | NADPH Oxidases - genetics | Hypertrophy, Right Ventricular - pathology | Hypertension, Pulmonary - drug therapy | Indoles | Hypertension, Pulmonary - enzymology | Disease Models, Animal | Signal Transduction | Mice, Inbred C57BL | NADPH Oxidases - antagonists & inhibitors | Enzyme Inhibitors - pharmacology | Rats | Familial Primary Pulmonary Hypertension | Hypertension, Pulmonary - genetics | Hypoxia - complications | Adventitia - drug effects | NADPH Oxidase 4 | Pulmonary Artery - drug effects | Fibroblasts - pathology | Hypertrophy, Right Ventricular - enzymology | Rats, Sprague-Dawley | Pulmonary Artery - enzymology | Animals | Hypertrophy, Right Ventricular - prevention & control | Adventitia - pathology | Mice | Hypertension, Pulmonary - etiology | Hypertension, Pulmonary - pathology | Pulmonary Artery - pathology | Cell Movement | Index Medicus
Journal Article
Circulation, ISSN 0009-7322, 07/2012, Volume 126, Issue 4, pp. 455 - 467
Background-Epigenetic programming, dynamically regulated by histone acetylation, is a key mechanism regulating cell proliferation and survival. Little is known... 
genetic | epigenesis | vorinostat | histone deacetylation | pulmonary | valproic acid | hypertension | TARGET | CELLS | APOPTOSIS | CARDIAC & CARDIOVASCULAR SYSTEMS | ACETYLATION | hypertension, pulmonary | epigenesis, genetic | PROLIFERATION | EMERGENCE | ARTERIAL-HYPERTENSION | PROSTATE-CANCER | IN-VIVO | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | EXPRESSION | Muscle, Smooth, Vascular - metabolism | Humans | Male | Valproic Acid - pharmacology | Pulmonary Artery - metabolism | Histone Deacetylase 1 - antagonists & inhibitors | Valproic Acid - therapeutic use | Hypertension, Pulmonary - drug therapy | Lung - metabolism | Hydroxamic Acids - pharmacology | Disease Models, Animal | Muscle, Smooth, Vascular - drug effects | Lung - pathology | Cells, Cultured | Rats | Histone Deacetylases - metabolism | Hypertension, Pulmonary - metabolism | Hypoxia - complications | Platelet-Derived Growth Factor - pharmacology | Pulmonary Artery - drug effects | Rats, Sprague-Dawley | Muscle, Smooth, Vascular - pathology | Animals | Lung - drug effects | Histone Deacetylase Inhibitors - pharmacology | Histone Deacetylases - drug effects | Hydroxamic Acids - therapeutic use | Cell Proliferation - drug effects | Histone Deacetylase Inhibitors - therapeutic use | Hypertension, Pulmonary - etiology | Pulmonary Artery - pathology | Histone Deacetylase 1 - metabolism | Cell proliferation | Divalproex | Care and treatment | Usage | Enzyme inhibitors | Physiological aspects | Research | Valproic acid | Health aspects | Pulmonary hypertension | Index Medicus | Abridged Index Medicus
Journal Article