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1. Full Text Matrix metalloproteinases and their inhibitors in vascular remodeling and vascular disease
by Raffetto, Joseph D and Khalil, Raouf A
Biochemical pharmacology, ISSN 0006-2952, 2008, Volume 75, Issue 2, pp. 346 - 359
Blood vessels | MMP | Extracellular matrix | Aneurysm | Varicose veins | TIMP | Life Sciences & Biomedicine | Pharmacology & Pharmacy | Science & Technology | Cardiology. Vascular system | Biological and medical sciences | Medical sciences | Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous | Blood and lymphatic vessels | Pharmacology. Drug treatments | Varicose Veins - etiology | Vascular Diseases - etiology | Blood Vessels - pathology | Humans | Vascular Diseases - enzymology | Pre-Eclampsia - etiology | Pre-Eclampsia - enzymology | Hypertension - etiology | Pregnancy | Atherosclerosis - etiology | Atherosclerosis - enzymology | Animals | Aortic Aneurysm, Abdominal - enzymology | Varicose Veins - enzymology | Matrix Metalloproteinase Inhibitors | Female | Matrix Metalloproteinases - physiology | Tissue Inhibitor of Metalloproteinases - physiology | Hypertension - enzymology | Coronary Restenosis - enzymology | Neovascularization, Physiologic | Aortic Aneurysm, Abdominal - etiology | Coronary Restenosis - etiology | Hypertension | Collagenases | Aneurysms | Nitric oxide | Prostanoids | Index Medicus | blood vessels | aneurysm | varicose veins | extracellular matrix
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2. Full Text Human Alanine-Glyoxylate Aminotransferase 2 Lowers Asymmetric Dimethylarginine and Protects from Inhibition of Nitric Oxide Production
by Roman N. Rodionov and Daryl J. Murry and Sarah F. Vaulman and Jeff W. Stevens and Steven R. Lentz
The Journal of biological chemistry, ISSN 0021-9258, 02/2010, Volume 285, Issue 8, pp. 5385 - 5391
Life Sciences & Biomedicine | Biochemistry & Molecular Biology | Science & Technology | Diabetes Mellitus - enzymology | Mitochondria - enzymology | Adenoviridae | Liver - enzymology | Heart Failure - enzymology | Humans | Kidney - enzymology | Citrulline - metabolism | Nitric Oxide Synthase - antagonists & inhibitors | Arginine - analogs & derivatives | Atherosclerosis - enzymology | Transaminases - metabolism | Hypertension - enzymology | Nitric Oxide - biosynthesis | Gene Expression | Chlorocebus aethiops | Transduction, Genetic | Transaminases - genetics | Hydrolysis | Animals | Mice | Nitric Oxide Synthase - metabolism | COS Cells | Endothelial Cells - enzymology | Arginine - metabolism | Index Medicus | Amino Acid | Mitochondria | ADMA | Nitric Oxide | Cell Biology | Endothelium | Nitric-Oxide Synthase
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3. Full Text Lysyl Oxidases Play a Causal Role in Vascular Remodeling in Clinical and Experimental Pulmonary Arterial Hypertension
by Nave, Alexander H and Mižíková, Ivana and Niess, Gero and Steenbock, Heiko and Reichenberger, Frank and Talavera, María L and Veit, Florian and Herold, Susanne and Mayer, Konstantin and Vadász, István and Weissmann, Norbert and Seeger, Werner and Brinckmann, Jürgen and Morty, Rory E
Arteriosclerosis, thrombosis, and vascular biology, ISSN 1079-5642, 07/2014, Volume 34, Issue 7, pp. 1446 - 1458
anoxia | muscle | pulmonary | protein-lysine 6-oxidase | hypertension | extracellular matrix | smooth | Peripheral Vascular Disease | Life Sciences & Biomedicine | Hematology | Cardiovascular System & Cardiology | Science & Technology | 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 | Index Medicus
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4. Full Text Hypoxia-Dependent Regulation of Nonphagocytic NADPH Oxidase Subunit NOX4 in the Pulmonary Vasculature
by Mittal, Manish and Roth, Markus and König, Peter and Hofmann, Simone and Dony, Eva and Goyal, Parag and Selbitz, Anne-Christin and Schermuly, Ralph Theo and Ghofrani, Hossein Ardeschir and Kwapiszewska, Grazyna and Kummer, Wolfgang and Klepetko, Walter and Hoda, Mir Ali Reza and Fink, Ludger and Hänze, Jörg and Seeger, Werner and Grimminger, Friedrich and Schmidt, Harald H.H.W and Weissmann, Norbert
Circulation research, ISSN 0009-7330, 08/2007, Volume 101, Issue 3, pp. 258 - 267
Vascular smooth muscle cell proliferation | Hypoxia | Hypoxic pulmonary vasoconstriction | NADPH oxidase | Pulmonary hypertension | Cardiac & Cardiovascular Systems | Peripheral Vascular Disease | Life Sciences & Biomedicine | Hematology | Cardiovascular System & Cardiology | Science & Technology | Fundamental and applied biological sciences. Psychology | Biological and medical sciences | Pulmonary hypertension. Acute cor pulmonale. Pulmonary embolism. Pulmonary vascular diseases | Medical sciences | Vertebrates: cardiovascular system | Pneumology | Membrane Glycoproteins - analysis | Oxygen - pharmacology | Protein Subunits | Tunica Media - pathology | Humans | Myocytes, Smooth Muscle - pathology | Hypertension, Pulmonary - physiopathology | Male | Oxygen - metabolism | RNA, Messenger - biosynthesis | RNA Interference | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Cell Division | Drug Design | Superoxides - metabolism | NADPH Oxidases - genetics | Female | Hypertension, Pulmonary - drug therapy | NADPH Oxidases - biosynthesis | Hypertension, Pulmonary - enzymology | Endoplasmic Reticulum - enzymology | Cells, Cultured - drug effects | Hypoxia - enzymology | Myocytes, Smooth Muscle - enzymology | NADPH Oxidases - analysis | RNA, Small Interfering - pharmacology | Enzyme Induction | Nitric Oxide - physiology | Hypoxia - complications | NADPH Oxidase 4 | Organ Specificity | NADPH Oxidase 2 | Transforming Growth Factor beta1 - physiology | Cells, Cultured - enzymology | Pulmonary Artery - enzymology | Pulmonary Artery - cytology | Animals | Hypoxia - physiopathology | Lung - blood supply | Chronic Disease | Hypertension, Pulmonary - etiology | NADPH Oxidases - physiology | Tunica Media - enzymology | Hypertrophy | Index Medicus
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5. Full Text Endothelial NADPH Oxidase-2 Promotes Interstitial Cardiac Fibrosis and Diastolic Dysfunction Through Proinflammatory Effects and Endothelial-Mesenchymal Transition
by Murdoch, Colin E and Chaubey, Sanjay and Zeng, Lingfang and Yu, Bin and Ivetic, Aleksander and Walker, Simon J and Vanhoutte, Davy and Heymans, Stephane and Grieve, David J and Cave, Alison C and Brewer, Alison C and Zhang, Min and Shah, Ajay M
Journal of the American College of Cardiology, ISSN 0735-1097, 06/2014, Volume 63, Issue 24, pp. 2734 - 2741
endothelial-mesenchymal transition | diastolic dysfunction | endothelium | NADPH (nicotinamide adenine dinucleotide phosphate) oxidase | angiotensin II | Cardiac & Cardiovascular Systems | Life Sciences & Biomedicine | Cardiovascular System & Cardiology | Science & Technology | 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 | Hypertension | Heart failure | Genotype & phenotype | Stroke | Heart attacks | Pathogenesis | Rodents | Cardiomyocytes | Variance analysis | Endothelium
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6. Full Text Expression patterns of RelA and c-mip are associated with different glomerular diseases following anti-VEGF therapy
by Izzedine, Hassan and Mangier, Melanie and Ory, Virginie and Zhang, Shao-Yu and Sendeyo, Kelhia and Bouachi, Khedidja and Audard, Vincent and Péchoux, Christine and Soria, Jean C and Massard, Christophe and Bahleda, Rastilav and Bourry, Edward and Khayat, David and Baumelou, Alain and Lang, Philippe and Ollero, Mario and Pawlak, Andre and Sahali, Djillali
Kidney international, ISSN 0085-2538, 2014, Volume 85, Issue 2, pp. 457 - 470
anti-VEGF | FSGS | NF-κB | c-mip | thrombotic microangiopathy | MCNS | Life Sciences & Biomedicine | Urology & Nephrology | Science & Technology | Glomerulosclerosis, Focal Segmental - enzymology | Predictive Value of Tests | Humans | Middle Aged | Male | Protein Kinase Inhibitors - adverse effects | Young Adult | Proteinuria - chemically induced | Renal Insufficiency - chemically induced | Base Sequence | Kidney Diseases - chemically induced | Glomerulosclerosis, Focal Segmental - chemically induced | Transcription, Genetic | Hypertension - enzymology | Angiogenesis Inhibitors - adverse effects | Binding Sites | Biomarkers - metabolism | Niacinamide - adverse effects | Kidney Glomerulus - pathology | Thrombotic Microangiopathies - enzymology | Mice, Knockout | Glomerulosclerosis, Focal Segmental - diagnosis | Adaptor Proteins, Signal Transducing | Nephrosis, Lipoid - chemically induced | Thrombotic Microangiopathies - diagnosis | Mice | Transcription Factor RelA - deficiency | Niacinamide - analogs & derivatives | Renal Insufficiency - enzymology | Renal Insufficiency - diagnosis | Vascular Endothelial Growth Factors - antagonists & inhibitors | Kidney Diseases - diagnosis | Molecular Sequence Data | Nephrosis, Lipoid - enzymology | Kidney Diseases - enzymology | Transcription Factor RelA - genetics | Case-Control Studies | Transfection | Phenylurea Compounds - adverse effects | Hypertension - chemically induced | Adult | Female | Proteinuria - diagnosis | Hypertension - diagnosis | Kidney Glomerulus - enzymology | Cell Line | Promoter Regions, Genetic | Nephrosis, Lipoid - diagnosis | Kidney Glomerulus - drug effects | Gene Expression Regulation | Carrier Proteins - genetics | Proteinuria - enzymology | Animals | Carrier Proteins - metabolism | Transcription Factor RelA - metabolism | Vascular Endothelial Growth Factors - metabolism | Aged | Thrombotic Microangiopathies - chemically induced | Index Medicus | Life Sciences | Biochemistry, Molecular Biology
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7. Full Text Decreased creatine kinase is linked to diastolic dysfunction in rats with right heart failure induced by pulmonary artery hypertension
by Fowler, Ewan D and Benoist, David and Drinkhill, Mark J and Stones, Rachel and Helmes, Michiel and Wüst, Rob C.I and Stienen, Ger J.M and Steele, Derek S and White, Ed
Journal of molecular and cellular cardiology, ISSN 0022-2828, 2015, Volume 86, pp. 1 - 8
Cardiovascular | Right ventricular failure | Creatine kinase | Diastolic sarcomere length | Monocrotaline | Pulmonary artery hypertension | Cardiac & Cardiovascular Systems | Life Sciences & Biomedicine | Cardiovascular System & Cardiology | Science & Technology | Cell Biology | Diastole | Calcium - metabolism | Heart Failure - enzymology | Humans | Rats | Myocardium - pathology | Heart Failure - pathology | Ventricular Dysfunction, Right - enzymology | Pulmonary Artery - enzymology | Sarcomeres - pathology | Myocytes, Cardiac - enzymology | Myocytes, Cardiac - pathology | Myocardium - enzymology | Animals | Creatine Kinase - biosynthesis | Adenosine Triphosphate - metabolism | Creatine Kinase - metabolism | Sarcomeres - enzymology | Hypertension, Pulmonary - pathology | Hypertension, Pulmonary - enzymology | Pulmonary Artery - pathology | Ventricular Dysfunction, Right - pathology | Heart failure | Hypertension | Index Medicus | Original
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8. Full Text Dimethylarginine dimethylaminohydrolase (DDAH): expression, regulation, and function in the cardiovascular and renal systems
by Fredrik Palm and Maristela L. Onozato and Zaiming Luo and Christopher S. Wilcox
American Journal of Physiology - Heart and Circulatory Physiology, ISSN 0363-6135, 12/2007, Volume 293, Issue 6, pp. 3227 - 3245
Hypertension | Asymmetric dimethylarginine | Nitric oxide synthase | Chronic kidney disease | Diabetes mellitus | Cardiac & Cardiovascular Systems | Physiology | Peripheral Vascular Disease | Life Sciences & Biomedicine | Cardiovascular System & Cardiology | Science & Technology | Amidohydrolases - metabolism | Diabetes Mellitus - enzymology | Amidohydrolases - genetics | Humans | Kidney - enzymology | Endothelium, Vascular - physiopathology | Nitric Oxide Synthase - antagonists & inhibitors | Kidney Diseases - enzymology | Cardiovascular Diseases - enzymology | Endothelium, Vascular - enzymology | Arginine - analogs & derivatives | Vasodilation | Gene Expression Regulation, Enzymologic | Animals | Endothelium-Dependent Relaxing Factors - metabolism | Isoenzymes - metabolism | Liver Diseases - enzymology | Nitric Oxide Synthase - metabolism | Nitric Oxide - metabolism | Arginine - metabolism | Kidney - physiopathology | Nephrology | Kidneys | Nitric oxide | Diabetes | Kidney diseases | Cardiology | Index Medicus
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