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Nature reviews. Cardiology, ISSN 1759-5002, 10/2019, Volume 16, Issue 10, pp. 578 - 579
Journal Article
Journal Article
Circulation Research, ISSN 0009-7330, 08/2019, Volume 125, Issue 6, pp. 590 - 605
RATIONALE:Endothelial dysfunction results in sustained and chronic vascular inflammation, which is central to atherosclerotic diseases. However,... 
atherosclerosis | endothelium | CARDIAC & CARDIOVASCULAR SYSTEMS | simvastatin | mice | DEFICIENCY | KLF2 | FLOW | REGULATOR | TRANSCRIPTION FACTOR FOXP1 | inflammasome | DISEASE | PERIPHERAL VASCULAR DISEASE | KRUPPEL-LIKE FACTOR-2 | DYSFUNCTION | DIFFERENTIATION | HEMATOLOGY | Blood circulation disorders | Genetic aspects | Research | Gene expression | Atherosclerosis | Index Medicus
Journal Article
Journal Article
Clinical and Experimental Pharmacology and Physiology, ISSN 0305-1870, 03/2008, Volume 35, Issue 3, pp. 310 - 316
1 In coronary artery disease, the typical atheromatous plaque consists of a lipid core containing various inflammatory cells and a fibrous cap composed mostly... 
atherosclerosis | glucoside | matrix metalloproteinase‐9 | b | rat | 2,3,4′,5‐tetrahydroxystilbene‐2 | matrix metalloproteinase‐2 | interleukin‐6 | C‐reactive protein | tumour necrosis factor‐a | Matrix metalloproteinase-9 | C-reactive protein | Tumour necrosis factor-α | Rat | 2,3,4′,5- tetrahydroxystilbene-2-O-β-D-glucoside | Atherosclerosis | Matrix metalloproteinase-2 | Interleukin-6 | RESVERATROL | matrix metalloproteinase-2 | PHYSIOLOGY | MYOCARDIAL-INFARCTION | matrix metalloproteinase-9 | HEART-FAILURE | RISK | NECROSIS-FACTOR-ALPHA | interleukin-6 | 2,3,4',5-tetrahydroxystilbene-2-O-beta-D-glucoside | INHIBITION | CARDIOVASCULAR-DISEASE | PHARMACOLOGY & PHARMACY | SMOOTH-MUSCLE-CELLS | EXTRACELLULAR-MATRIX | tumour necrosis factor-alpha | Gene Expression Regulation, Enzymologic - drug effects | Atherosclerosis - drug therapy | Stilbenes - administration & dosage | Stilbenes - therapeutic use | Simvastatin | Rats | Male | Rats, Sprague-Dawley | Dose-Response Relationship, Drug | Animals | Glucosides - administration & dosage | Anti-Inflammatory Agents, Non-Steroidal - therapeutic use | Inflammation - drug therapy | Anti-Inflammatory Agents, Non-Steroidal - administration & dosage | Glucosides - therapeutic use | Matrix Metalloproteinases - metabolism | Matrix Metalloproteinases, metabolism | Anti-Inflammatory Agents, Non-Steroidal, therapeutic use | Stilbenes, administration and dosage | Anti-Inflammatory Agents, Non-Steroidal, administration and dosage | Glucosides, therapeutic use | Stilbenes, therapeutic use | Inflammation, drug therapy | Atherosclerosis, drug therapy | Gene Expression Regulation, Enzymologic, drug effects | Glucosides, administration and dosage | Index Medicus
Journal Article
Journal Article
Journal Article
Cancer Letters, ISSN 0304-3835, 2016, Volume 385, pp. 215 - 224
Abstract Malignant mesothelioma (MM) frequently exhibits Hippo signaling pathway inactivation (HPI) mainly due to NF2 and/or LATS2 mutations, which leads to... 
Hematology, Oncology and Palliative Medicine | Cancer stem cell | YAP | Malignant mesothelioma | Hippo pathway | Statin | CD44 | PLEURAL MESOTHELIOMA | ORGAN SIZE CONTROL | CANCER STEM-CELLS | BREAST-CANCER | ZOLEDRONIC ACID | ONCOLOGY | SIGNALING PATHWAY | DEUBIQUITINASE BAP1 | TUMOR-SUPPRESSOR | CANDIDATE ONCOGENE | MEVALONATE PATHWAY | Lung Neoplasms - drug therapy | Neurofibromin 2 - genetics | Phosphorylation | Fatty Acids, Monounsaturated - pharmacology | Mesothelioma - pathology | Neoplastic Stem Cells - drug effects | Humans | Lung Neoplasms - metabolism | Gene Expression Regulation, Neoplastic | Lung Neoplasms - pathology | Phosphoproteins - metabolism | Simvastatin - pharmacology | Dose-Response Relationship, Drug | Fluvastatin | Transfection | Neoplastic Stem Cells - metabolism | RNA Interference | Time Factors | Tumor Suppressor Proteins - genetics | Hyaluronan Receptors - metabolism | Neoplastic Stem Cells - pathology | Ubiquitin Thiolesterase - metabolism | Indoles - pharmacology | Transcription, Genetic | Antineoplastic Agents - pharmacology | Binding Sites | Neurofibromin 2 - metabolism | Protein-Serine-Threonine Kinases - metabolism | Lung Neoplasms - genetics | Promoter Regions, Genetic | Tumor Suppressor Proteins - metabolism | Neoplasm Invasiveness | Protein-Serine-Threonine Kinases - genetics | Mesothelioma - genetics | Phosphoproteins - genetics | Mevalonic Acid - metabolism | Ubiquitin Thiolesterase - genetics | Hyaluronan Receptors - genetics | Mesothelioma - drug therapy | Cell Movement - drug effects | Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology | Mesothelioma - metabolism | Signal Transduction - drug effects | Adaptor Proteins, Signal Transducing - genetics | Cell Line, Tumor | Cell Proliferation - drug effects | Mutation | Adaptor Proteins, Signal Transducing - metabolism | Medical colleges | Mesothelioma | School construction | Statins | Stem cells | Medical research | Statistical analysis | Biosynthesis | Breast cancer | Metastasis | Gene expression | Experiments | Proteins | Insects | Medical prognosis | Cell cycle | Tumorigenesis | Tumors | Index Medicus
Journal Article
PLoS ONE, ISSN 1932-6203, 08/2018, Volume 13, Issue 8, pp. e0202827 - e0202827
The major drawback of current anti-angiogenic therapies is drug resistance, mainly caused by overexpression of the transcription factor, hypoxia-inducible... 
OXIDATIVE STRESS | DISRUPTING AGENT | MULTIDISCIPLINARY SCIENCES | L-DOPA | TUMOR-ASSOCIATED MACROPHAGES | LIPOSOMAL PREDNISOLONE PHOSPHATE | HIF-1-ALPHA EXPRESSION | TRANSCRIPTION FACTOR | CANCER-THERAPY | PROGRESSION | L-TYROSINE | Tumor Microenvironment - drug effects | Xanthones - therapeutic use | Simvastatin - therapeutic use | Macrophages - pathology | Neoplasm Invasiveness | Coculture Techniques | Melanoma, Experimental - drug therapy | Neovascularization, Pathologic | Angiogenesis Inhibitors - pharmacology | Melanoma, Experimental - pathology | Drug Resistance, Neoplasm | Simvastatin - pharmacology | Xanthones - pharmacology | Cell Movement - drug effects | Animals | Cell Communication - drug effects | Angiogenesis Inhibitors - therapeutic use | Macrophages - drug effects | Cell Proliferation - drug effects | Mice | Drug Therapy, Combination | Drug Screening Assays, Antitumor | Proteins | Simvastatin | Melanoma | Development and progression | Drug resistance | Acetic acid | Macrophages | Organic acids | Antilipemic agents | Cell proliferation | Cell culture | Oxidative stress | Biotechnology | Transcription factors | Leukocyte migration | Deceleration | Arginase | Polyamines | Cell interactions | Cancer therapies | Mimicry | Anticancer properties | Angiogenesis | Lipophilic | Tumor necrosis factor-TNF | Inhibition | Growth factors | Hypoxia-inducible factors | Medical research | Enzymes | Phenotypes | Cytokines | Geology | Tumor cells | Interdisciplinary aspects | Gene expression | Pathology | Immunosuppression | Acids | Hypoxia | Antitumor activity | Combined treatment | Molecular biology | Cell migration | Cancer | Tumors | Index Medicus
Journal Article