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Nature Cell Biology, ISSN 1465-7392, 08/2015, Volume 17, Issue 8, pp. 994 - 1003
The use of human pluripotent stem cells for in vitro disease modelling and clinical applications requires protocols that convert these cells into relevant... 
DIRECTED DIFFERENTIATION | IN-VIVO | MOUSE | DEFINITIVE ENDODERM | GROWTH-FACTOR | HUMAN BLASTOCYSTS | STROMAL CELLS | WNT | CULTURE | LINES | CELL BIOLOGY | Coculture Techniques | Humans | Endothelial Cells - transplantation | Glycogen Synthase Kinase 3 beta | Cell Lineage - drug effects | Dose-Response Relationship, Drug | Human Umbilical Vein Endothelial Cells - physiology | Transfection | Time Factors | Gene Expression Regulation, Developmental | Transcription, Genetic | Myocytes, Smooth Muscle - drug effects | Proto-Oncogene Proteins c-sis - pharmacology | Myocytes, Smooth Muscle - transplantation | Vascular Endothelial Growth Factor A - pharmacology | Endothelial Cells - physiology | Muscle, Smooth, Vascular - physiology | Muscle, Smooth, Vascular - drug effects | Biomarkers - metabolism | Cell Line | Induced Pluripotent Stem Cells - enzymology | Induced Pluripotent Stem Cells - drug effects | Induced Pluripotent Stem Cells - physiology | Glycogen Synthase Kinase 3 - antagonists & inhibitors | Myocytes, Smooth Muscle - enzymology | Induced Pluripotent Stem Cells - transplantation | Myocytes, Smooth Muscle - physiology | Gene Expression Profiling - methods | Muscle, Smooth, Vascular - transplantation | Glycogen Synthase Kinase 3 - metabolism | Mice, SCID | Muscle, Smooth, Vascular - cytology | Metabolomics - methods | Bone Morphogenetic Protein 4 - pharmacology | Phenotype | Animals | Wnt Signaling Pathway - drug effects | Cell Differentiation - drug effects | Mice, Inbred NOD | Protein Kinase Inhibitors - pharmacology | Endothelial Cells - enzymology | Muscle, Smooth, Vascular - enzymology | Neovascularization, Physiologic | Endothelial Cells - drug effects | Usage | Cell research | Growth | Stem cells | Muscle cells | Research | Cell differentiation | Endothelium
Journal Article
Circulation Research, ISSN 0009-7330, 05/2012, Volume 110, Issue 11, pp. 1484 - 1497
RATIONALE:Pulmonary arterial hypertension (PAH) is a lethal syndrome characterized by pulmonary vascular obstruction caused, in part, by pulmonary artery... 
mitotic checkpoint | cyclin B1/cyclin-dependent kinase 1 | mitochondrial fission | hypoxia-inducible factor-1 | mitochondrial division inhibitor-1 | CARDIAC & CARDIOVASCULAR SYSTEMS | ENTRY | INDUCIBLE FACTOR 1-ALPHA | HYPOXIA | DRP1 | PATHWAY | ARTERIAL-HYPERTENSION | ENDOTHELIAL-CELLS | GENE-EXPRESSION | GERMLINE MUTATIONS | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | K+ CHANNELS | Antihypertensive Agents - pharmacology | Humans | Monocrotaline | Male | Cyclin B1 - metabolism | Cobalt | Hypertension, Pulmonary - therapy | CDC2 Protein Kinase - metabolism | RNA Interference | Time Factors | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Mitochondrial Proteins - metabolism | Myocytes, Smooth Muscle - drug effects | Hypertension, Pulmonary - enzymology | Disease Models, Animal | Muscle, Smooth, Vascular - drug effects | Myocytes, Smooth Muscle - enzymology | Dynamins - genetics | Rats | Familial Primary Pulmonary Hypertension | Hypoxia - complications | Rats, Sprague-Dawley | Pulmonary Artery - enzymology | Cell Cycle Checkpoints | GTP Phosphohydrolases - metabolism | GTP Phosphohydrolases - genetics | Mitochondria, Muscle - drug effects | Enzyme Activation | Hypertension, Pulmonary - etiology | Muscle, Smooth, Vascular - enzymology | Dynamins - metabolism | Phosphorylation | Microtubule-Associated Proteins - genetics | Microtubule-Associated Proteins - metabolism | Serine | Myocytes, Smooth Muscle - pathology | Mitochondrial Proteins - genetics | Case-Control Studies | Transfection | Quinazolinones - pharmacology | Mitochondria, Muscle - enzymology | Mitochondria, Muscle - pathology | Cells, Cultured | Muscle, Smooth, Vascular - pathology | Animals | Mitosis - drug effects | Glycolysis | Cell Proliferation - drug effects | Hypertension, Pulmonary - pathology | Pulmonary Artery - pathology | Genetic Therapy - methods | Hypoxia-inducible factor 1 | CDK1-cyclin B1 | Mitochondrial division inhibitor-1 (Mdivi-1) | Mitochondrial fission | Mitotic check point
Journal Article
Journal of the American Heart Association, ISSN 2047-9980, 02/2016, Volume 5, Issue 2, p. n/a
Background The choline‐derived metabolite trimethylamine N‐oxide (TMAO) has been demonstrated to contribute to atherosclerosis and is associated with coronary... 
atherosclerosis | cardiovascular disease | inflammation | endothelial cell | nuclear factor‐κB signaling | vascular smooth muscle cell | leukocyte adhesion | trimethylamine N‐oxide | Endothelial cell | Trimethylamine N-oxide | Nuclear factor-κB signaling | Atherosclerosis | Cardiovascular disease | Leukocyte adhesion | Vascular smooth muscle cell | Inflammation | MICROBIAL-METABOLISM | CARDIAC & CARDIOVASCULAR SYSTEMS | HYDROSTATIC-PRESSURE | HEART-FAILURE | ADHESION MOLECULES | trimethylamine N-oxide | HUMAN ENDOTHELIAL-CELLS | L-CARNITINE | LYSOPHOSPHATIDIC ACID | CARDIOVASCULAR-DISEASE | PHOSPHATIDYLCHOLINE | nuclear factor-kappa B signaling | Atherosclerosis - genetics | Coculture Techniques | Humans | Myocytes, Smooth Muscle - pathology | Aortitis - enzymology | NF-kappa B - metabolism | Aortitis - chemically induced | Leukocytes - enzymology | Atherosclerosis - enzymology | Receptors, LDL - deficiency | Female | Aortitis - pathology | Myocytes, Smooth Muscle - drug effects | Aorta - enzymology | Disease Models, Animal | Muscle, Smooth, Vascular - drug effects | Receptors, LDL - genetics | Atherosclerosis - pathology | Genetic Predisposition to Disease | Myocytes, Smooth Muscle - enzymology | Aorta - drug effects | Atherosclerosis - chemically induced | Mice, Inbred C57BL | Cells, Cultured | Gene Expression Regulation | Aortitis - genetics | Cell Adhesion - drug effects | Mice, Knockout | Aorta - pathology | Muscle, Smooth, Vascular - pathology | Phenotype | Animals | Signal Transduction - drug effects | Choline | Leukocytes - drug effects | Enzyme Activation | Methylamines - toxicity | Endothelial Cells - pathology | Endothelial Cells - enzymology | Muscle, Smooth, Vascular - enzymology | Endothelial Cells - drug effects | Mitogen-Activated Protein Kinases - metabolism
Journal Article
Science Translational Medicine, ISSN 1946-6234, 12/2015, Volume 7, Issue 318, p. 318ra200
Autoantibodies to components of apoptotic cells, such as anti-perlecan antibodies, contribute to rejection in organ transplant recipients. However, mechanisms... 
SOLID-ORGAN TRANSPLANTATION | MEDICINE, RESEARCH & EXPERIMENTAL | ACUTE KIDNEY INJURY | SYSTEMIC-LUPUS-ERYTHEMATOSUS | CORONARY-ARTERY DISEASE | EXTRACELLULAR VESICLES | ANTIVIMENTIN ANTIBODIES | PERLECAN FRAGMENT LG3 | NON-HLA ANTIBODIES | MESENCHYMAL STEM-CELLS | CHRONIC ALLOGRAFT NEPHROPATHY | CELL BIOLOGY | Cell-Derived Microparticles - enzymology | Humans | Muscle, Smooth, Vascular - immunology | Immunity, Humoral | Ischemia - immunology | Time Factors | Peptide Fragments - immunology | Exosomes - immunology | Acute Kidney Injury - immunology | Proteomics - methods | Graft Rejection - pathology | Proteasome Endopeptidase Complex - immunology | Ischemia - pathology | Aorta - transplantation | Disease Models, Animal | Biomarkers - metabolism | Acute Kidney Injury - pathology | Myocytes, Smooth Muscle - enzymology | Rats | Aorta - immunology | Acute Kidney Injury - enzymology | Aorta - pathology | Human Umbilical Vein Endothelial Cells - enzymology | Exosomes - enzymology | Human Umbilical Vein Endothelial Cells - pathology | Mice, Inbred BALB C | Graft Rejection - immunology | Proteasome Endopeptidase Complex - metabolism | Muscle, Smooth, Vascular - enzymology | Ischemia - enzymology | Myocytes, Smooth Muscle - pathology | Human Umbilical Vein Endothelial Cells - immunology | Exosomes - pathology | Autoantibodies - biosynthesis | Allografts | Cell-Derived Microparticles - pathology | Kidney Tubules, Proximal - enzymology | Aorta - enzymology | Graft Rejection - enzymology | Kidney Tubules, Proximal - immunology | Kidney Tubules, Proximal - pathology | Peptide Fragments - metabolism | Mice, Inbred C57BL | Cells, Cultured | Heparan Sulfate Proteoglycans - immunology | Autoantibodies - immunology | Muscle, Smooth, Vascular - pathology | Animals | Apoptosis - immunology | Cell-Derived Microparticles - immunology | Heparan Sulfate Proteoglycans - metabolism | Myocytes, Smooth Muscle - immunology
Journal Article
Journal Article
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
Journal Article
Circulation, ISSN 0009-7322, 01/2010, Volume 121, Issue 1, pp. 98 - 109
Background-Pulmonary arterial hypertension is a progressive proliferative vasculopathy of the small pulmonary arteries that is characterized by a primary... 
Hypoxia | Nitric oxide | Pulmonary artery smooth muscle cells | Xanthine oxidoreductase | Monocrotaline sodium | hypoxia | nitric oxide | xanthine oxidoreductase | ISCHEMIA/REPERFUSION INJURY | CARDIAC & CARDIOVASCULAR SYSTEMS | ORGANIC NITRATES | monocrotaline sodium | ACTIVATED-PROTEIN-KINASE | CELL-PROLIFERATION | EXERCISE CAPACITY | pulmonary artery smooth muscle cells | SYNTHASE | L-ARGININE | IN-VIVO | PERIPHERAL VASCULAR DISEASE | ISCHEMIA-REPERFUSION | HEMATOLOGY | EXPRESSION | Xanthine Dehydrogenase - metabolism | Hypoxia - drug therapy | Xanthine Dehydrogenase - antagonists & inhibitors | Male | Hypertension, Pulmonary - chemically induced | Hypoxia - metabolism | Sodium Nitrite - pharmacology | Cyclin-Dependent Kinase Inhibitor p21 - genetics | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Hypertension, Pulmonary - drug therapy | Myocytes, Smooth Muscle - drug effects | Myocytes, Smooth Muscle - cytology | Disease Models, Animal | Myocytes, Smooth Muscle - enzymology | Mice, Inbred C57BL | Cells, Cultured | Administration, Inhalation | Rats | Hypertension, Pulmonary - metabolism | Monocrotaline - toxicity | Rats, Sprague-Dawley | Cell Division - drug effects | Mice, Knockout | Pulmonary Artery - cytology | Animals | Mice | Nitric Oxide - metabolism | Sodium Nitrite - pharmacokinetics | Chronic Disease | Cell proliferation | Control | Nitrites | Physiological aspects | Smooth muscle | Research | Pulmonary hypertension
Journal Article
Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 06/2016, Volume 36, Issue 6, pp. 1085 - 1089
Journal Article
Circulation Research, ISSN 0009-7330, 01/2016, Volume 118, Issue 2, pp. 230 - 240
RATIONALE:Genetic variation at the chromosome 9p21 cardiovascular risk locus has been associated with peripheral artery disease, but its mechanism remains... 
atherosclerosis | smooth muscle cells | genetic variation | peripheral artery disease | cyclin-dependent kinase inhibitor p15 | pathologic angiogenesis | CARDIAC & CARDIOVASCULAR SYSTEMS | PROTEIN | MYOCARDIAL-INFARCTION | AORTIC-ANEURYSM | RISK INTERVAL | CHROMOSOME 9P21 VARIANTS | HIC-5 | GENE | PERIPHERAL ARTERY-DISEASE | TUMOR-SUPPRESSOR | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | EXPRESSION | Hindlimb | Atherosclerosis - genetics | Humans | Transforming Growth Factor beta1 - metabolism | Neovascularization, Pathologic | Male | Muscle, Smooth, Vascular - physiopathology | Cell Hypoxia | Atherosclerosis - enzymology | Transfection | RNA Interference | Time Factors | Cyclin-Dependent Kinase Inhibitor p15 - genetics | Carotid Arteries - enzymology | Female | Disease Models, Animal | Muscle, Skeletal - blood supply | Smad7 Protein - metabolism | Atherosclerosis - pathology | Coronary Vessels - pathology | Genetic Predisposition to Disease | Coronary Vessels - enzymology | Signal Transduction | Cyclin-Dependent Kinase Inhibitor p15 - deficiency | Myocytes, Smooth Muscle - enzymology | Mice, Inbred C57BL | Cells, Cultured | Atherosclerosis - mortality | Transforming Growth Factor beta1 - genetics | Chromosomes, Human, Pair 9 | Mice, Knockout | Phenotype | Animals | Carotid Arteries - pathology | Cyclin-Dependent Kinase Inhibitor p15 - metabolism | Muscle, Smooth, Vascular - enzymology | Neovascularization, Physiologic | cardiovascular disease CDKN2B | Pathophysiology | Risk Factors | angiogenesis | Atherosclerosis | TGFβ | Peripheral Vascular Disease | 9p21 | Gene Expression and Regulation
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