X
Search Filters
Format Format
Format Format
X
Sort by Item Count (A-Z)
Filter by Count
Journal Article (594) 594
Publication (80) 80
Book / eBook (2) 2
Book Chapter (2) 2
Book Review (2) 2
Conference Proceeding (2) 2
Newspaper Article (1) 1
more...
Subjects Subjects
Subjects Subjects
X
Sort by Item Count (A-Z)
Filter by Count
animals (542) 542
male (332) 332
rats (268) 268
index medicus (258) 258
peripheral vascular disease (226) 226
muscle, smooth, vascular - enzymology (193) 193
humans (187) 187
disease models, animal (168) 168
cells, cultured (155) 155
mice (154) 154
hematology (142) 142
cardiac & cardiovascular systems (131) 131
rats, sprague-dawley (131) 131
carotid arteries - enzymology (129) 129
muscle, smooth, vascular - pathology (125) 125
carotid artery injuries - enzymology (122) 122
carotid artery injuries - pathology (118) 118
carotid arteries - pathology (113) 113
atherosclerosis (107) 107
tunica intima - pathology (106) 106
time factors (102) 102
expression (98) 98
mice, knockout (96) 96
myocytes, smooth muscle - enzymology (96) 96
mice, inbred c57bl (95) 95
female (93) 93
muscle, smooth, vascular - drug effects (92) 92
restenosis (89) 89
hyperplasia (85) 85
tunica intima - enzymology (85) 85
carotid arteries (82) 82
proliferation (77) 77
cell proliferation (72) 72
injury (72) 72
neointima (72) 72
myocytes, smooth muscle - pathology (71) 71
phosphorylation (69) 69
physiology (67) 67
muscle, smooth, vascular - cytology (66) 66
rats, wistar (66) 66
endothelium, vascular - enzymology (64) 64
immunohistochemistry (63) 63
nitric oxide (63) 63
transfection (63) 63
signal transduction (59) 59
smooth-muscle-cells (58) 58
neointima formation (56) 56
smooth-muscle cells (56) 56
article (54) 54
dose-response relationship, drug (54) 54
enzyme activation (54) 54
rabbits (54) 54
cell movement (53) 53
balloon injury (52) 52
activation (51) 51
carotid arteries - drug effects (51) 51
endothelium (51) 51
in-vivo (50) 50
migration (50) 50
myocytes, smooth muscle - drug effects (50) 50
rat carotid-artery (50) 50
carotid artery injuries - genetics (49) 49
enzyme inhibitors - pharmacology (49) 49
oxidative stress (49) 49
tunica intima - drug effects (49) 49
inflammation (48) 48
intimal hyperplasia (48) 48
nitric-oxide synthase (48) 48
apoptosis (47) 47
gene expression (46) 46
medicine, research & experimental (45) 45
vascular injury (42) 42
angioplasty (41) 41
gene transfer techniques (41) 41
surgery (41) 41
cell proliferation - drug effects (40) 40
endothelial-cells (40) 40
matrix metalloproteinases (40) 40
pharmacology & pharmacy (40) 40
carotid artery injuries (39) 39
carotid artery, common - enzymology (39) 39
carotid artery, common - pathology (39) 39
catheterization - adverse effects (39) 39
muscle, smooth, vascular - metabolism (39) 39
rat (39) 39
research article (39) 39
analysis (38) 38
biochemistry & molecular biology (38) 38
growth-factor (37) 37
inhibition (37) 37
rna interference (37) 37
in-vitro (36) 36
signal transduction - drug effects (36) 36
angioplasty, balloon - adverse effects (35) 35
cell movement - drug effects (35) 35
medicine (35) 35
rna, messenger - metabolism (35) 35
up-regulation (35) 35
carotid-artery (34) 34
smooth muscle (34) 34
more...
Library Location Library Location
Language Language
Publication Date Publication Date
Click on a bar to filter by decade
Slide to change publication date range


Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 08/2016, Volume 36, Issue 8, pp. 1549 - 1557
OBJECTIVE—Cathepsin S (CatS) participates in atherogenesis through several putative mechanisms. The ability of cathepsins to modify histone tail is likely to... 
neointimal formation | vascular remodeling | cathepsin S | HDAC6 | MIGRATION | ATHEROSCLEROTIC PLAQUES | PROLIFERATION | CYSTEINE PROTEASE CATHEPSINS | HISTONE DEACETYLASES | METABOLISM | DISEASE | PERIPHERAL VASCULAR DISEASE | SMOOTH-MUSCLE-CELLS | NEOVASCULARIZATION | HEMATOLOGY | EXPRESSION | Phosphorylation | Vascular Remodeling | Cell Proliferation | Toll-Like Receptor 2 - genetics | Myocytes, Smooth Muscle - pathology | Male | Protease Inhibitors - pharmacology | Neointima | Transfection | RNA Interference | Carotid Artery Injuries - genetics | p38 Mitogen-Activated Protein Kinases - metabolism | Proto-Oncogene Proteins c-akt - metabolism | Phosphatidylinositol 3-Kinase - metabolism | Wound Healing - drug effects | Carotid Artery Injuries - pathology | Cathepsins - antagonists & inhibitors | Disease Models, Animal | Histone Deacetylases - genetics | Signal Transduction | Histone Deacetylase 6 | Myocytes, Smooth Muscle - enzymology | Cells, Cultured | Genotype | Histone Deacetylases - metabolism | Toll-Like Receptor 2 - metabolism | Mice, Knockout | Cell Cycle Checkpoints | Muscle, Smooth, Vascular - pathology | Phenotype | Animals | Carotid Artery Injuries - enzymology | Cathepsins - genetics | Carotid Artery, Common - enzymology | Cathepsins - metabolism | Carotid Artery, Common - drug effects | Carotid Artery, Common - pathology | Histone Deacetylase Inhibitors - pharmacology | Muscle, Smooth, Vascular - enzymology | Cathepsins - deficiency | Cell Movement | 10054 | 10012 | Basic Sciences
Journal Article
Circulation Research, ISSN 0009-7330, 03/2009, Volume 104, Issue 5, pp. 688 - 698
ABSTRACT—The migration of vascular smooth muscle cells (VSMCs) plays an essential role during the development of atherosclerosis and restenosis. Extensive... 
Extracellular matrix | Metalloproteinase | Neointima formation | Vascular smooth muscle cell migration | neointima formation | RNA INTERFERENCE | CARDIAC & CARDIOVASCULAR SYSTEMS | metalloproteinase | vascular smooth muscle cell migration | MECHANISMS | OLIGOMERIC MATRIX PROTEIN | HYPERPLASIA | INHIBITION | DISEASE | GROWTH | MATRIX-METALLOPROTEINASE-9 | DEGRADATION | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | extracellular matrix | Tumor Necrosis Factor-alpha - metabolism | Hyperplasia | Glycoproteins - metabolism | Myocytes, Smooth Muscle - pathology | Male | NF-kappa B - metabolism | Transcription Factor AP-1 - metabolism | Carotid Artery Injuries - etiology | Matrilin Proteins | RNA Interference | Time Factors | Carotid Arteries - enzymology | Extracellular Matrix Proteins - metabolism | Carotid Artery Injuries - pathology | Disease Models, Animal | Transduction, Genetic | Myocytes, Smooth Muscle - enzymology | Proto-Oncogene Proteins c-sis | Cells, Cultured | Rats | Tunica Intima - enzymology | Rats, Sprague-Dawley | ADAM Proteins - metabolism | Muscle, Smooth, Vascular - pathology | Platelet-Derived Growth Factor - metabolism | Animals | Carotid Artery Injuries - enzymology | Tunica Intima - pathology | ADAMTS7 Protein | Catheterization - adverse effects | Carotid Arteries - pathology | ADAM Proteins - genetics | Muscle, Smooth, Vascular - enzymology | Cell Movement | RNA, Small Interfering - metabolism
Journal Article
Circulation, ISSN 0009-7322, 2015, Volume 131, Issue 13, pp. 1191 - 1201
Journal Article
Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 11/2012, Volume 32, Issue 11, pp. 2662 - 2669
OBJECTIVE—Abnormal proliferation and migration of vascular smooth muscle cells (SMCs) are the key events in the progression of neointima formation in response... 
Yes-associated protein | Smooth muscle | Neointima formation | Phenotypic modulation | neointima formation | MYOCARDIN | HIPPO-YAP PATHWAY | ALPHA-ACTIN EXPRESSION | TRANSCRIPTION | smooth muscle | phenotypic modulation | ORGAN SIZE | GROWTH | SERUM RESPONSE FACTOR | yes-associated protein | CELL DIFFERENTIATION | PERIPHERAL VASCULAR DISEASE | SIZE-CONTROL | HEMATOLOGY | BINDING | Cell Proliferation | Vascular System Injuries - genetics | Myocytes, Smooth Muscle - pathology | Vascular System Injuries - enzymology | Male | Phosphoproteins - metabolism | Gene Knockdown Techniques | Vascular System Injuries - pathology | Neointima | Transfection | RNA Interference | Time Factors | Apoptosis Regulatory Proteins - genetics | Carotid Arteries - enzymology | Carotid Artery Injuries - genetics | Aorta - enzymology | Carotid Artery Injuries - pathology | Disease Models, Animal | Myocytes, Smooth Muscle - enzymology | Mice, Inbred C57BL | Cells, Cultured | Gene Expression Regulation | Rats | Genotype | Phosphoproteins - genetics | Vascular System Injuries - prevention & control | Rats, Sprague-Dawley | Apoptosis Regulatory Proteins - metabolism | Aorta - pathology | Carotid Artery Injuries - prevention & control | Muscle, Smooth, Vascular - pathology | Phenotype | Animals | Carotid Artery Injuries - enzymology | Adaptor Proteins, Signal Transducing - genetics | Carotid Arteries - pathology | Mice | Adaptor Proteins, Signal Transducing - metabolism | Muscle, Smooth, Vascular - enzymology | Cell Movement
Journal Article
Atherosclerosis, ISSN 0021-9150, 2015, Volume 241, Issue 1, pp. 111 - 120
Abstract In vitro , insulin has mitogenic effects on vascular smooth muscle cells (VSMC) but also has protective effects on endothelial cells by stimulating... 
Cardiovascular | Endothelial nitric oxide synthase | Neointima | Angioplasty | Insulin | Re-endothelialization | MIGRATION | ACTIVATION | PHOSPHORYLATION | MECHANISMS | RAT CAROTID-ARTERY | INTIMAL HYPERPLASIA | BALLOON INJURY | PERIPHERAL VASCULAR DISEASE | SMOOTH-MUSCLE-CELLS | EXPRESSION | IN-STENT RESTENOSIS | Femoral Artery - pathology | Phosphorylation | Carotid Artery Injuries - drug therapy | Drug Implants | Vascular System Injuries - enzymology | Male | Vascular System Injuries - drug therapy | Nitric Oxide Synthase Type III - deficiency | Dose-Response Relationship, Drug | Femoral Artery - enzymology | Vascular System Injuries - pathology | Femoral Artery - injuries | Time Factors | Aorta, Thoracic - drug effects | Nitric Oxide Synthase Type III - metabolism | Aorta, Thoracic - pathology | Carotid Artery Injuries - pathology | Disease Models, Animal | Vascular System Injuries - physiopathology | Vasodilator Agents - pharmacology | Mice, Inbred C57BL | Enzyme Inhibitors - pharmacology | Aorta, Thoracic - injuries | Insulin - administration & dosage | Re-Epithelialization - drug effects | Femoral Artery - drug effects | Nitric Oxide Synthase Type III - genetics | Rats, Sprague-Dawley | Mice, Knockout | Nitric Oxide Synthase Type III - antagonists & inhibitors | Aorta, Thoracic - enzymology | Cell Movement - drug effects | Animals | Carotid Artery Injuries - enzymology | Signal Transduction - drug effects | Carotid Artery Injuries - physiopathology | Carotid Artery, Common - enzymology | Carotid Artery, Common - drug effects | Carotid Artery, Common - pathology | Vasodilation - drug effects | Growth | Nitric oxide | Analysis | Physiological aspects | Statistics | Endothelium
Journal Article
Atherosclerosis, ISSN 0021-9150, 2012, Volume 222, Issue 2, pp. 375 - 381
Highlights ► We investigated the mechanism whereby resveratrol, a red wine polyphenol, decreases restenosis. ► We used two models of restenosis, arterial... 
Cardiovascular | Restenosis | Endothelial nitric oxide synthase | Neointima | Proliferation | Resveratrol | SURVIVAL | REENDOTHELIALIZATION | ACTIVATION | CARDIAC & CARDIOVASCULAR SYSTEMS | METABOLISM | INSULIN-RESISTANCE | PERIPHERAL VASCULAR DISEASE | MICE | HYPERTENSION | Carotid Arteries - drug effects | Femoral Artery - pathology | Platelet Endothelial Cell Adhesion Molecule-1 - genetics | Stilbenes - administration & dosage | Vascular System Injuries - genetics | Carotid Artery Injuries - drug therapy | Vascular System Injuries - enzymology | Male | Stilbenes - pharmacology | RNA, Messenger - metabolism | Vascular System Injuries - drug therapy | Nitric Oxide Synthase Type III - deficiency | Femoral Artery - enzymology | Vascular System Injuries - pathology | Femoral Artery - injuries | Time Factors | Matrix Metalloproteinase 9 - genetics | Carotid Arteries - enzymology | Carotid Artery Injuries - genetics | Nitric Oxide Synthase Type III - metabolism | Aorta - enzymology | Carotid Artery Injuries - pathology | Disease Models, Animal | NG-Nitroarginine Methyl Ester - pharmacology | Cardiovascular Agents - administration & dosage | Administration, Oral | Aorta - drug effects | Mice, Inbred C57BL | Enzyme Inhibitors - pharmacology | Gene Expression Regulation | Rats | Aorta - injuries | Femoral Artery - drug effects | Nitric Oxide Synthase Type III - genetics | Rats, Sprague-Dawley | Cardiovascular Agents - pharmacology | Mice, Knockout | Nitric Oxide Synthase Type III - antagonists & inhibitors | Aorta - pathology | Animals | Carotid Artery Injuries - enzymology | Carotid Arteries - pathology | Cell Proliferation - drug effects | Mice | Nitrogen oxide | Wine | Analysis | Nitric oxide | Atherosclerosis | Physiological aspects | Universities and colleges | Endothelium
Journal Article
Journal Article
Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 02/2015, Volume 35, Issue 2, pp. 368 - 377
OBJECTIVE—An aneurysm is an inflammatory vascular condition. Phosphatidylinositol 3-kinases δ is highly expressed in leukocytes, and play a key role in innate... 
aneurysm | matrix metalloproteinases-12 | activator protein-1 | extracellular matrix | ACTIVATION | MATRIX METALLOPROTEINASE-12 | CELL ANTIGEN | PHOSPHOINOSITIDE 3-KINASE | DEFICIENCY | ABDOMINAL AORTIC-ANEURYSM | INFLAMMATION | TOLL-LIKE RECEPTORS | PERIPHERAL VASCULAR DISEASE | METALLOELASTASE | HEMATOLOGY | NF-KAPPA-B | Aortic Aneurysm, Abdominal - chemically induced | Transcription Factor AP-1 - genetics | Carotid Artery, Common - surgery | Macrophages, Peritoneal - pathology | Male | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Transcription Factor AP-1 - metabolism | Aorta, Abdominal - drug effects | Ligation | Transfection | Phosphatidylinositol 3-Kinases - deficiency | RNA Interference | Carotid Artery Injuries - genetics | Aorta, Abdominal - pathology | Macrophages, Peritoneal - drug effects | Aortic Aneurysm, Abdominal - pathology | Extracellular Matrix Proteins - metabolism | Carotid Artery Injuries - pathology | Disease Models, Animal | Cell Line | Calcium Chloride | Adenine - analogs & derivatives | Signal Transduction | Extracellular Matrix Proteins - genetics | Mice, Inbred C57BL | Macrophages, Peritoneal - enzymology | Adenine - pharmacology | Aortic Aneurysm, Abdominal - genetics | Matrix Metalloproteinase 12 - metabolism | Aorta, Abdominal - enzymology | Mice, Knockout | Gene Expression Regulation, Enzymologic | Phosphatidylinositol 3-Kinases - genetics | Tumor Necrosis Factor-alpha - pharmacology | Animals | Aortic Aneurysm, Abdominal - enzymology | Carotid Artery Injuries - enzymology | Carotid Artery, Common - enzymology | Carotid Artery, Common - drug effects | Carotid Artery, Common - pathology | Protein Kinase Inhibitors - pharmacology | Enzyme Activation | Aorta, Abdominal - surgery | Quinazolines - pharmacology
Journal Article
American Journal of Physiology - Heart and Circulatory Physiology, ISSN 0363-6135, 2015, Volume 309, Issue 11, pp. H1894 - H1903
Epoxyeicosatrienoic acids (EETs) have beneficial effects on cardiovascular disease. Soluble epoxide hydrolase (sEH) metabolizes EETs to less active diols, thus... 
Soluble epoxide hydrolase inhibitor | Vascular smooth muscle cell | Neointima formation | Migration | Atherosclerosis | atherosclerosis | neointima formation | EICOSANOIDS | CARDIAC & CARDIOVASCULAR SYSTEMS | PHYSIOLOGY | VIVO | MODEL | soluble epoxide hydrolase inhibitor | ENDOTHELIUM IN-VITRO | INHIBITION | migration | PERIPHERAL VASCULAR DISEASE | vascular smooth muscle cell | INDUCED CARDIAC-HYPERTROPHY | DIFFERENTIATION | EPOXYEICOSATRIENOIC ACIDS | EXPRESSION | MOLECULAR-MECHANISMS | Vascular Remodeling | Cell Proliferation | Atherosclerosis - genetics | Humans | Middle Aged | Myocytes, Smooth Muscle - pathology | Cell Dedifferentiation | Male | Coronary Artery Disease - enzymology | Young Adult | Atherosclerosis - enzymology | Neointima | Transfection | Piperidines - pharmacology | Time Factors | Coronary Artery Disease - pathology | Adult | Female | Carotid Artery Injuries - genetics | Myocytes, Smooth Muscle - drug effects | Proto-Oncogene Proteins c-sis - pharmacology | Carotid Artery Injuries - pathology | Disease Models, Animal | Muscle, Smooth, Vascular - drug effects | Atherosclerosis - pathology | Signal Transduction | Myocytes, Smooth Muscle - enzymology | Cells, Cultured | Enzyme Inhibitors - pharmacology | Rats, Sprague-Dawley | Disease Progression | Epoxide Hydrolases - genetics | Carotid Artery Injuries - therapy | Cell Movement - drug effects | Muscle, Smooth, Vascular - pathology | Phenotype | Animals | Carotid Artery Injuries - enzymology | Eicosanoids - metabolism | Adolescent | Coronary Artery Disease - genetics | Aged | Phenylurea Compounds - pharmacology | Epoxide Hydrolases - metabolism | Epoxide Hydrolases - antagonists & inhibitors | Muscle, Smooth, Vascular - enzymology | Atherosclerosis - prevention & control | Enzymes | Smooth muscle | Hydrolases | Platelet-derived growth factor | Analysis | Development and progression | Muscle cells | Observations | Health aspects | Cell migration
Journal Article
Journal of Vascular Surgery, ISSN 0741-5214, 2015, Volume 64, Issue 4, pp. 1074 - 1083
Objective Effective treatments against restenosis after percutaneous transluminal angioplasty and stenting are largely lacking. Human tissue kallikrein gene... 
Surgery | Carotid Arteries - drug effects | Tumor Necrosis Factor-alpha - metabolism | Phosphorylation | Carotid Stenosis - prevention & control | Humans | Hyperplasia | Transforming Growth Factor beta1 - metabolism | Tumor Necrosis Factor-alpha - genetics | Myocytes, Smooth Muscle - pathology | Carotid Artery Injuries - drug therapy | Male | Smad3 Protein - metabolism | Interleukin-1beta - genetics | Kallikreins - administration & dosage | Angioplasty, Balloon - adverse effects | Angiography, Digital Subtraction | Foam Cells - drug effects | Neointima | Time Factors | Carotid Stenosis - genetics | Interleukin-1beta - metabolism | Diet, High-Fat | Inflammation Mediators - metabolism | Carotid Arteries - enzymology | Carotid Artery Injuries - genetics | Nitric Oxide Synthase Type III - metabolism | Myocytes, Smooth Muscle - drug effects | Foam Cells - pathology | Carotid Artery Injuries - pathology | Disease Models, Animal | Muscle, Smooth, Vascular - drug effects | Rabbits | Kallikreins - pharmacology | Drug Administration Schedule | Myocytes, Smooth Muscle - enzymology | Urine - chemistry | Smad2 Protein - metabolism | Carotid Stenosis - pathology | Foam Cells - enzymology | Kallikreins - urine | Administration, Intravenous | Muscle, Smooth, Vascular - pathology | Animals | Carotid Artery Injuries - enzymology | Signal Transduction - drug effects | Carotid Arteries - pathology | Carotid Stenosis - enzymology | Muscle, Smooth, Vascular - enzymology
Journal Article
Circulation Research, ISSN 0009-7330, 09/2009, Volume 105, Issue 6, pp. 537 - 544
RATIONALE:Endothelial progenitor cells (EPCs, defined as sca-1flk-1lin mononuclear blood cells) contribute to vascular repair. The role of hypoxia and reactive... 
Oxidative stress | NADPH oxidase | Superoxide | ACTIVATION | CARDIAC & CARDIOVASCULAR SYSTEMS | COA REDUCTASE INHIBITORS | BONE-MARROW | TYROSINE PHOSPHATASES | SIGNAL-TRANSDUCTION | SYNTHASE | NAD(P)H OXIDASE | ERYTHROPOIETIN RECEPTOR | HINDLIMB ISCHEMIA | PERIPHERAL VASCULAR DISEASE | SMOOTH-MUSCLE-CELLS | superoxide | HEMATOLOGY | oxidative stress | Protein Tyrosine Phosphatase, Non-Receptor Type 11 - metabolism | Leukocytes, Mononuclear - metabolism | Antigens, Ly | Reactive Oxygen Species - metabolism | Membrane Glycoproteins - metabolism | NADPH Oxidases - metabolism | Vascular Endothelial Growth Factor Receptor-2 | STAT5 Transcription Factor - metabolism | Stem Cells - enzymology | Bone Marrow Transplantation | Carotid Arteries - enzymology | NADPH Oxidases - genetics | Carotid Artery Injuries - genetics | Erythropoietin - metabolism | Wound Healing - genetics | NADH, NADPH Oxidoreductases - metabolism | Carotid Artery Injuries - pathology | NADH, NADPH Oxidoreductases - genetics | Hypoxia - enzymology | Gene Expression Regulation - genetics | Cells, Cultured | Signal Transduction - genetics | NADPH Oxidase 2 | NADPH Oxidase 1 | Membrane Glycoproteins - genetics | Mice, Knockout | Membrane Proteins | Leukocytes, Mononuclear - pathology | Hypoxia - genetics | Animals | Carotid Artery Injuries - enzymology | Hypoxia - pathology | Stem Cells - pathology | Leukocytes, Mononuclear - enzymology | Carotid Arteries - pathology | Mice | Endothelial Cells - pathology | Endothelial Cells - enzymology
Journal Article
Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 04/2012, Volume 32, Issue 4, pp. 943 - 954
OBJECTIVE—The adventitia is increasingly recognized as an important player during the development of intimal hyperplasia. However, the mechanism of adventitial... 
apoptosis | restenosis | carotid arteries | intimal hyperplasia | vascular biology | PROGENITOR CELLS | ARTERIAL INJURY | NEOINTIMA FORMATION | DEFICIENT MICE | IN-VIVO | BALLOON INJURY | PERIPHERAL VASCULAR DISEASE | SMOOTH-MUSCLE-CELLS | GENE-TRANSFER | HEMATOLOGY | Genetic Therapy | Fibroblasts - enzymology | Cell Proliferation | Chemokine CCL2 - immunology | Hyperplasia | Myocytes, Smooth Muscle - pathology | Muscle, Smooth, Vascular - immunology | Male | Transfection | Time Factors | Carotid Artery Injuries - genetics | Chemokine CCL2 - metabolism | Angioplasty, Balloon | Carotid Artery Injuries - pathology | Disease Models, Animal | Connective Tissue - pathology | Myocytes, Smooth Muscle - enzymology | Cells, Cultured | Rats | Connective Tissue - immunology | Fibroblasts - pathology | Rats, Sprague-Dawley | Carotid Artery Injuries - therapy | Protein Kinase C-delta - metabolism | Antibodies - administration & dosage | Connective Tissue - enzymology | Muscle, Smooth, Vascular - pathology | Receptors, CCR2 - metabolism | Animals | Carotid Artery Injuries - enzymology | Myocytes, Smooth Muscle - immunology | Fibroblasts - immunology | Carotid Artery Injuries - immunology | Chemokine CCL2 - antagonists & inhibitors | Muscle, Smooth, Vascular - enzymology | Protein Kinase C-delta - genetics | Apoptosis | Cell Movement | Culture Media, Conditioned - metabolism | PKCδ | MCP-1 | myofibroblasts | CCR2
Journal Article
Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 03/2017, Volume 37, Issue 3, pp. 476 - 484
Journal Article
Circulation Research, ISSN 0009-7330, 07/2015, Volume 117, Issue 4, pp. 376 - 387
Journal Article