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Arteriosclerosis, thrombosis, and vascular biology, ISSN 1524-4636, 02/2017, Volume 37, Issue 2, pp. 328 - 340
OBJECTIVE—The calcium composition of atherosclerotic plaque is thought to be associated with increased risk for cardiovascular events, but whether plaque... 
atherosclerosis | coronary artery disease | macrophages | inflammation | biomarkers | Peripheral Vascular Disease | Life Sciences & Biomedicine | Hematology | Cardiovascular System & Cardiology | Science & Technology | Up-Regulation | Prognosis | Apolipoproteins E - deficiency | Atherosclerosis - genetics | Humans | Myocytes, Smooth Muscle - pathology | rac GTP-Binding Proteins - deficiency | rac GTP-Binding Proteins - metabolism | Male | Coronary Artery Disease - enzymology | Atherosclerosis - enzymology | Transfection | Interleukin-1beta - metabolism | rac GTP-Binding Proteins - genetics | Coronary Artery Disease - pathology | Inflammation Mediators - metabolism | Aortic Diseases - prevention & control | Vascular Calcification - mortality | Female | Vascular Calcification - enzymology | Aortic Diseases - enzymology | Interleukin 1 Receptor Antagonist Protein - pharmacology | Aorta - enzymology | Aortic Diseases - pathology | Atherosclerosis - pathology | Coronary Vessels - pathology | Genetic Predisposition to Disease | Coronary Vessels - enzymology | Macrophages - pathology | Signal Transduction | Myocytes, Smooth Muscle - enzymology | Mice, Inbred C57BL | Cells, Cultured | Neuropeptides - metabolism | Coronary Artery Disease - mortality | Plaque, Atherosclerotic | Vascular Calcification - pathology | Macrophages - enzymology | Mice, Knockout | Aorta - pathology | Aortic Diseases - genetics | Muscle, Smooth, Vascular - pathology | Phenotype | Animals | Apolipoproteins E - genetics | Muscle, Smooth, Vascular - enzymology | Atherosclerosis - prevention & control | rac1 GTP-Binding Protein - metabolism | Index Medicus
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 | Cardiac & Cardiovascular Systems | Life Sciences & Biomedicine | Cardiovascular System & Cardiology | Science & Technology | 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 | Index Medicus
Journal Article
Journal Article
Clinical and experimental pharmacology & physiology, ISSN 0305-1870, 10/2008, Volume 35, Issue 10, pp. 1156 - 1163
SUMMARY 1 Fabry disease results from an X‐linked mutation in the lysosomal α‐galactosidase A (Gla) gene. Defective Gla results in multi‐organ accumulation of... 
Fabry disease | endothelium | globotriaosylceramide | α‐galactosidase A | Globotriaosylceramide | α-galactosidase A | Endothelium | Pharmacology & Pharmacy | Physiology | Life Sciences & Biomedicine | Science & Technology | alpha-Galactosidase - genetics | Vascular Diseases - pathology | Blood Pressure - genetics | Fabry Disease - genetics | Male | Fabry Disease - enzymology | alpha-Galactosidase - physiology | Endothelium, Vascular - enzymology | Fabry Disease - pathology | Cell Membrane - pathology | Blood Pressure - physiology | Cell Membrane - metabolism | Aorta, Thoracic - pathology | Disease Models, Animal | Mice, Inbred C57BL | Aorta, Thoracic - metabolism | Vascular Diseases - genetics | Vascular Diseases - enzymology | Mice, Knockout | Aorta, Thoracic - enzymology | Cell Membrane - enzymology | Animals | Endothelial Cells - cytology | Endothelium, Vascular - metabolism | Glycosphingolipids - metabolism | Endothelium, Vascular - pathology | Mice | Endothelial Cells - pathology | In Vitro Techniques | Endothelial Cells - enzymology | Vascular Diseases, pathology | Aorta, Thoracic, pathology | Endothelial Cells, cytology | Endothelium, Vascular, metabolism | Cell Membrane, enzymology | Aorta, Thoracic, metabolism | Endothelial Cells, pathology | alpha-Galactosidase, genetics | Glycosphingolipids, metabolism | Endothelial Cells, enzymology | Endothelium, Vascular, enzymology | Endothelium, Vascular, pathology | Cell Membrane, pathology | Blood Pressure, physiology | Cell Membrane, metabolism | Vascular Diseases, enzymology | Fabry Disease, pathology | Fabry Disease, enzymology | Aorta, Thoracic, enzymology | Blood Pressure, genetics | alpha-Galactosidase, physiology | Vascular Diseases, genetics | Fabry Disease, genetics | Index Medicus
Journal Article
Arteriosclerosis, thrombosis, and vascular biology, ISSN 1079-5642, 07/2006, Volume 26, Issue 7, pp. 1579 - 1585
OBJECTIVE—To study the distribution of group V secretory phospholipase A2 (sPLA2) in human and mouse lesions and compare its expression by human vascular... 
Atherogenesis | Phospholipase | Lipoprotein-retention | Inflammation | Proteoglycans | Blood Vessels - pathology | Humans | Phospholipases A - metabolism | Phospholipases A2 | RNA, Messenger - metabolism | Lipopolysaccharide Receptors - analysis | Arteries - metabolism | Atherosclerosis - enzymology | Drug Interactions | Carotid Artery Diseases - pathology | Isoenzymes - metabolism | Blood Vessels - enzymology | Phospholipases A - pharmacology | Aorta - enzymology | Macrophages - immunology | Atherosclerosis - pathology | Isoenzymes - genetics | Blood - drug effects | Enzyme Induction | Proteoglycans - metabolism | Recombinant Proteins - pharmacology | Macrophages - enzymology | Immunohistochemistry - methods | Group II Phospholipases A2 | Animals | Diet | Phospholipases A - genetics | Carotid Artery Diseases - enzymology | Staining and Labeling | Isoenzymes - pharmacology | Mice | Lipoproteins - drug effects | Index Medicus | Macrophages/enzymology/immunology | RNA | Recombinant Proteins/pharmacology | MEDICIN OCH HÄLSOVETENSKAP | Carotid Artery Diseases/enzymology/pathology | Aorta/enzymology | Immunohistochemistry/methods | Blood/drug effects | Blood Vessels/enzymology/pathology | Lipoproteins/drug effects | Phospholipases A/genetics/metabolism/pharmacology | MEDICAL AND HEALTH SCIENCES | Antigens | Proteoglycans/metabolism | Isoenzymes/genetics/metabolism/pharmacology | CD14/analysis | Arteries/metabolism | Messenger/metabolism | Atherosclerosis/enzymology/pathology
Journal Article
Arteriosclerosis, thrombosis, and vascular biology, ISSN 1524-4636, 03/2018, Volume 38, Issue 3, pp. 509 - 519
OBJECTIVE—Tissue macrophages induce and perpetuate proinflammatory responses, thereby promoting metabolic and cardiovascular disease. Lipoprotein lipase (LpL),... 
Monocytes | Leukocytosis | Hematopoiesis | Bone marrow | Lipoprotein lipase | Colony-stimulating factors | Macrophages | Peripheral Vascular Disease | Life Sciences & Biomedicine | Hematology | Cardiovascular System & Cardiology | Science & Technology | Cell Proliferation | Atherosclerosis - genetics | Hyperlipoproteinemia Type I - blood | Aortic Diseases - blood | Myeloid Progenitor Cells - enzymology | Intercellular Signaling Peptides and Proteins - metabolism | Atherosclerosis - enzymology | Hyperlipoproteinemia Type I - pathology | Diet, High-Fat | Monocytes - pathology | Aortic Diseases - enzymology | Myelopoiesis | Aorta - enzymology | Aortic Diseases - pathology | Disease Models, Animal | Atherosclerosis - pathology | Cytokines - metabolism | Macrophages - pathology | Signal Transduction | Lipoprotein Lipase - genetics | Hyperlipoproteinemia Type I - enzymology | Myeloid Progenitor Cells - pathology | Lipoprotein Lipase - deficiency | Hyperlipoproteinemia Type I - genetics | Macrophages - enzymology | Mice, Knockout | Triglycerides - metabolism | Aorta - pathology | Atherosclerosis - blood | Monocytes - enzymology | Aortic Diseases - genetics | Animals | Index Medicus | monocytes | hematopoiesis | macrophages | white blood cells | lipoprotein lipase | colony-stimulating factors | bone marrow | leukocytosis | Atherosclerosis Inflammation Lipids and Cholesterol Vascular Biology
Journal Article
Atherosclerosis, ISSN 0021-9150, 07/2017, Volume 262, pp. 113 - 122
Journal Article
Molecular cell, ISSN 1097-2765, 11/2011, Volume 44, Issue 4, pp. 545 - 558
Journal Article
Arteriosclerosis, thrombosis, and vascular biology, ISSN 1079-5642, 02/2016, Volume 36, Issue 2, pp. 295 - 307
OBJECTIVE—Oxidative stress is considered a hallmark of atherosclerosis. In particular, the superoxide-generating type 1 NADPH oxidase (NOX1) has been shown to... 
atherosclerosis | endothelial cells | diabetes mellitus | NADPH oxidase | reactive oxygen species | Peripheral Vascular Disease | Life Sciences & Biomedicine | Hematology | Cardiovascular System & Cardiology | Science & Technology | Inflammation - pathology | Vascular Remodeling | Apolipoproteins E - deficiency | Membrane Glycoproteins - metabolism | Oxidative Stress | Atherosclerosis - genetics | Humans | NADPH Oxidases - metabolism | Male | Case-Control Studies | NADPH Oxidases - deficiency | Atherosclerosis - enzymology | Transfection | RNA Interference | Time Factors | Inflammation Mediators - metabolism | Superoxides - metabolism | Aortic Diseases - prevention & control | NADPH Oxidases - genetics | Aortic Diseases - enzymology | NADH, NADPH Oxidoreductases - metabolism | Aorta - enzymology | Aortic Diseases - pathology | Disease Models, Animal | Fibrillar Collagens - metabolism | Atherosclerosis - pathology | Cytokines - metabolism | Signal Transduction | Cells, Cultured | NADPH Oxidase 4 | Plaque, Atherosclerotic | NADPH Oxidase 2 | NADPH Oxidase 1 | Hydrogen Peroxide - metabolism | Mice, Knockout | Aorta - pathology | Aortic Diseases - genetics | Animals | Apolipoproteins E - genetics | Inflammation - genetics | Inflammation - prevention & control | Endothelial Cells - pathology | Endothelial Cells - enzymology | Inflammation - enzymology | Atherosclerosis - prevention & control | Index Medicus
Journal Article
Arteriosclerosis, thrombosis, and vascular biology, ISSN 1524-4636, 06/2016, Volume 36, Issue 6, pp. 1122 - 1131
OBJECTIVE—The c-Jun NH2-terminal kinases (JNK) are regulated by a wide variety of cellular stresses and have been implicated in apoptotic signaling.... 
atherosclerosis | apoptosis | macrophages | MAP kinase signaling system | endoplasmic reticulum stress | Peripheral Vascular Disease | Life Sciences & Biomedicine | Hematology | Cardiovascular System & Cardiology | Science & Technology | Mitogen-Activated Protein Kinase 8 - antagonists & inhibitors | Apoptosis - drug effects | Bone Marrow Cells - enzymology | Atherosclerosis - genetics | Mitogen-Activated Protein Kinase 9 - genetics | PTEN Phosphohydrolase - antagonists & inhibitors | Atherosclerosis - enzymology | Hypercholesterolemia - enzymology | Diet, High-Fat | Bone Marrow Transplantation | Receptors, LDL - deficiency | bcl-Associated Death Protein - metabolism | Bone Marrow Cells - drug effects | Mitogen-Activated Protein Kinase 8 - genetics | Aortic Diseases - enzymology | Proto-Oncogene Proteins c-akt - metabolism | Aorta - enzymology | Aortic Diseases - pathology | Disease Models, Animal | Receptors, LDL - genetics | Atherosclerosis - pathology | Genetic Predisposition to Disease | Macrophages - pathology | Signal Transduction | Cell Survival | Aorta - drug effects | Mice, Inbred C57BL | Bone Marrow Cells - pathology | Cells, Cultured | PTEN Phosphohydrolase - metabolism | Plaque, Atherosclerotic | Mitogen-Activated Protein Kinase 9 - deficiency | Macrophages - enzymology | Mice, Knockout | Aorta - pathology | Mitogen-Activated Protein Kinase 8 - deficiency | Aortic Diseases - genetics | Phenotype | Animals | Endoplasmic Reticulum Stress | Mitogen-Activated Protein Kinase 9 - antagonists & inhibitors | Macrophages - drug effects | Protein Kinase Inhibitors - pharmacology | Hypercholesterolemia - genetics | Index Medicus
Journal Article