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The New England Journal of Medicine, ISSN 0028-4793, 12/2013, Volume 369, Issue 25, pp. 2391 - 2405
Journal Article
American Journal of Respiratory Cell and Molecular Biology, ISSN 1044-1549, 01/2014, Volume 50, Issue 1, pp. 170 - 179
Journal Article
The New England Journal of Medicine, ISSN 0028-4793, 02/2015, Volume 372, Issue 7, pp. 601 - 612
Journal Article
Journal of Cellular and Molecular Medicine, ISSN 1582-1838, 03/2018, Volume 22, Issue 3, pp. 1792 - 1804
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
American Journal of Respiratory Cell and Molecular Biology, ISSN 1044-1549, 2014, Volume 50, Issue 3, pp. 614 - 625
Acute lung injury (ALI) is a severe hypoxemic respiratory insufficiency associated with lung leak, diffuse alveolar damage, inflammation, and loss of lung... 
Acute lung injury | Gene delivery | Asymmetric dimethylarginine | Dimethylarginine dimethylaminohydrolase II | Nitrative stress | dimethylarginine dimethylaminohydrolase II | NITRIC-OXIDE SYNTHASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | acute lung injury | CELL BIOLOGY | gene delivery | DDAH/ADMA PATHWAY | CARDIOVASCULAR RISK-FACTOR | RESPIRATORY SYSTEM | INFLAMMATION | ENDOTHELIAL-CELLS | IN-VIVO | nitrative stress | DYSFUNCTION | INHIBITOR | NF-KAPPA-B | asymmetric dimethylarginine | Genetic Therapy | Up-Regulation | Capillary Permeability | Oxidative Stress | Humans | Microvessels - pathology | Acute Lung Injury - genetics | Male | Acute Lung Injury - enzymology | Arginine - analogs & derivatives | Lipopolysaccharides | Lung - enzymology | Transfection | Time Factors | Acute Lung Injury - prevention & control | Superoxides - metabolism | Pulmonary Edema - prevention & control | Microvessels - enzymology | Disease Models, Animal | Amidohydrolases - metabolism | Pulmonary Edema - genetics | Lung - pathology | Amidohydrolases - genetics | Mice, Inbred C57BL | Cells, Cultured | Pulmonary Edema - chemically induced | Animals | Acute Lung Injury - chemically induced | Pulmonary Edema - enzymology | Peroxynitrous Acid - metabolism | Mice | Bronchoalveolar Lavage Fluid - chemistry | Endothelial Cells - pathology | Lung - blood supply | Endothelial Cells - enzymology | Arginine - metabolism | Proteins | Studies | Cell culture | Rodents | Mortality | Permeability | Recruitment | Original Research
Journal Article
American Journal of Physiology - Lung Cellular and Molecular Physiology, ISSN 1040-0605, 2015, Volume 309, Issue 12, pp. L1410 - L1419
Journal Article
Journal Article
American Journal of Respiratory Cell and Molecular Biology, ISSN 1044-1549, 2014, Volume 50, Issue 5, pp. 942 - 952
Heat shock protein (hsp) 90 inhibition attenuates NF-kappa B activation and blocks inflammation. However, the precise mechanism of NF-kappa B regulation by... 
NF-κB | Human lung microvascular endothelial cells | Heat shock protein 90 inhibitor | CAMP response element binding protein binding protein | LPS | human lung microvascular endothelial cells | COMPLEX | cAMP response element binding protein binding protein | heat shock protein 90 inhibitor | PHOSPHORYLATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | BARRIER FUNCTION | CBP/P300 | ALPHA | INDUCTION | P65 | COACTIVATORS | CELL BIOLOGY | NF-kappa B | RESPIRATORY SYSTEM | INFLAMMATION | EXPRESSION | Phosphorylation | Humans | Microvessels - metabolism | NF-kappa B - metabolism | I-kappa B Proteins - metabolism | I-kappa B Proteins - genetics | Ubiquitination | HSP90 Heat-Shock Proteins - genetics | Lung - metabolism | Active Transport, Cell Nucleus | Promoter Regions, Genetic | NF-kappa B - antagonists & inhibitors | Histone Deacetylases - genetics | Endothelial Cells - metabolism | Cells, Cultured | Microvessels - drug effects | Histone Deacetylases - metabolism | Down-Regulation - drug effects | Lactams, Macrocyclic - pharmacology | Benzoquinones - pharmacology | Histones - genetics | NF-kappa B - genetics | HSP90 Heat-Shock Proteins - antagonists & inhibitors | Lung - drug effects | Lipopolysaccharides - pharmacology | HSP90 Heat-Shock Proteins - metabolism | Histones - metabolism | Endothelial Cells - drug effects | Original Research
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 02/2014, Volume 289, Issue 8, pp. 4710 - 4722
Journal Article
Infection, ISSN 0300-8126, 10/2015, Volume 43, Issue 5, pp. 589 - 593
Journal Article