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Hypertension, ISSN 0194-911X, 2014, Volume 63, Issue 6, pp. 1241 - 1250
Connective tissue growth factor (CTGF) is involved in the pathogenesis of various fibrotic disorders. However, its role in the heart is not clear. To... 
Hypertension | Inflammation | S100 proteins | Angiotensin II | MECHANISMS | MYELOID-RELATED PROTEIN-14 | RAGE | MAPK | MYELOID-RELATED-PROTEIN-8/14 | INHIBITION | inflammation | angiotensin II | PERIPHERAL VASCULAR DISEASE | TNF-ALPHA | DYSFUNCTION | hypertension | NF-KAPPA-B | EXPRESSION | Immunohistochemistry | Calgranulin B - metabolism | Oligonucleotide Array Sequence Analysis | Myocytes, Cardiac - immunology | Calgranulin A - genetics | Inflammation - metabolism | Myocardium - metabolism | Antibodies - immunology | Antigens, Ly - metabolism | Calgranulin A - immunology | Hypertension - genetics | Cytokines - genetics | Neutrophils - metabolism | Receptor for Advanced Glycation End Products | Fibroblasts - metabolism | Animals, Newborn | Angiotensin II - pharmacology | Neutrophils - drug effects | Toll-Like Receptor 4 - genetics | Hypertension - immunology | Toll-Like Receptor 4 - immunology | Reverse Transcriptase Polymerase Chain Reaction | Toll-Like Receptor 4 - metabolism | Myocytes, Cardiac - drug effects | Fibroblasts - drug effects | Myocytes, Cardiac - metabolism | Fibroblasts - immunology | Mice | Receptors, Immunologic - genetics | Myocardium - immunology | Calgranulin A - metabolism | Transcriptome - immunology | Calgranulin B - immunology | Hypertension - prevention & control | Calgranulin B - genetics | Receptors, Immunologic - immunology | Cytokines - immunology | CD11b Antigen - immunology | Cytokines - metabolism | Mice, Inbred C57BL | Cells, Cultured | Neutrophils - immunology | Myocardium - pathology | Inflammation - immunology | Transcriptome - drug effects | Angiotensin II - immunology | Antibodies - pharmacology | Animals | Antigens, Ly - immunology | Inflammation - genetics | CD11b Antigen - metabolism | Receptors, Immunologic - metabolism
Journal Article
Journal Article
Journal of Immunology, ISSN 0022-1767, 07/2015, Volume 195, Issue 2, pp. 672 - 682
Cardiac dysfunction is a major consequence of sepsis/septic shock and contributes to the high mortality of sepsis. Innate and inflammatory responses mediated... 
IMMUNITY | ACTIVATION | PLAYERS | ROLES | INJURY | MICE | KAPPA-B | IMMUNOLOGY | MODULATION | PROTECTS | Interleukin-1 Receptor-Associated Kinases - genetics | Myocardium - immunology | Carotid Arteries | Genetic Vectors - administration & dosage | Myocytes, Cardiac - immunology | NF-kappa B - immunology | Male | Sepsis - complications | TNF Receptor-Associated Factor 6 - antagonists & inhibitors | TNF Receptor-Associated Factor 6 - immunology | Lipopolysaccharides - antagonists & inhibitors | Heart Failure - therapy | Interleukin-1 Receptor-Associated Kinases - immunology | Heart Failure - immunology | Lentivirus - genetics | TNF Receptor-Associated Factor 6 - genetics | Heart Failure - etiology | Macrophages - immunology | Cytokines - immunology | Disease Models, Animal | NF-kappa B - antagonists & inhibitors | Sepsis - immunology | Macrophages - pathology | Signal Transduction | Mice, Inbred C57BL | Gene Expression Regulation | Heart Failure - genetics | Myocardium - pathology | Immunity, Innate | MicroRNAs - immunology | Sepsis - genetics | Myocytes, Cardiac - pathology | Administration, Intravenous | Animals | Myocytes, Cardiac - drug effects | NF-kappa B - genetics | Interleukin-1 Receptor-Associated Kinases - antagonists & inhibitors | Sepsis - therapy | Lipopolysaccharides - pharmacology | Macrophages - drug effects | Mice | MicroRNAs - genetics | Cytokines - antagonists & inhibitors | Primary Cell Culture | Cytokines - biosynthesis | microRNA-146a | NF-κB | cardiac function | TRAF6 | sepsis
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 05/2017, Volume 127, Issue 5, pp. 1600 - 1612
The cardiac extracellular matrix (ECM) not only provides mechanical support, but also transduces essential molecular signals in health and disease. Following... 
ISCHEMIA-REPERFUSION INJURY | MEDICINE, RESEARCH & EXPERIMENTAL | VOLUME OVERLOAD | HEART-FAILURE | CHRONIC PRESSURE-OVERLOAD | LEFT-VENTRICULAR DILATION | MATRICELLULAR PROTEINS | SMOOTH-MUSCLE-CELLS | ANGIOTENSIN-II | CARDIAC FIBROSIS | MICE LACKING OSTEOPONTIN | Inflammation - pathology | Leukocytes - pathology | Myocardium - immunology | Myocytes, Cardiac - immunology | Humans | Extracellular Matrix - immunology | Extracellular Matrix - metabolism | Stress, Mechanical | Heart Failure, Diastolic - metabolism | Myocardial Infarction - immunology | Leukocytes - immunology | Intercellular Signaling Peptides and Proteins - metabolism | Signal Transduction - immunology | Inflammation - metabolism | Myocardial Infarction - pathology | Myocardium - metabolism | Extracellular Matrix Proteins - metabolism | Myocardium - pathology | Inflammation - immunology | Myocardial Infarction - metabolism | Heart Failure, Diastolic - pathology | Myocytes, Cardiac - pathology | Animals | Extracellular Matrix Proteins - immunology | Heart Failure, Diastolic - immunology | Myocytes, Cardiac - metabolism | Extracellular Matrix - pathology | Leukocytes - metabolism | Intercellular Signaling Peptides and Proteins - immunology | Extracellular matrix | Care and treatment | Research | Regeneration (Biology) | Heart attack | Heart failure | Hypertension | Myocardial infarction | Heart attacks | Pathogenesis | Spatial discrimination | Cardiomyocytes | Inflammation | Metabolism | Proteins | Ischemia | Collagen | Rodents | Fibroblasts | Plastics | Growth factors | Heart diseases | Binding sites
Journal Article
Nature Communications, ISSN 2041-1723, 11/2016, Volume 7, Issue 1, p. 13344
Diabetes mellitus (DM) encompasses a multitude of secondary disorders, including heart disease. One of the most frequent and potentially life threatening... 
ACTIVATION | MYOCARDIAL-INFARCTION | INSULIN-RESISTANCE | MULTIDISCIPLINARY SCIENCES | TOLL-LIKE RECEPTORS | NLRP3 INFLAMMASOME | SARCOPLASMIC-RETICULUM | HUMAN MONOCYTES | VENTRICULAR REPOLARIZATION | NALP3 INFLAMMASOME | CONVERTING-ENZYME | Potassium - metabolism | Toll-Like Receptor 2 - genetics | Calcium - metabolism | Myocytes, Cardiac - immunology | Receptors, Interleukin-1 - genetics | Caspase 1 - metabolism | Interleukin-1beta - genetics | Action Potentials | NLR Family, Pyrin Domain-Containing 3 Protein - genetics | Inflammasomes - antagonists & inhibitors | Interleukin-1beta - metabolism | Arrhythmias, Cardiac - immunology | Tachycardia, Ventricular - metabolism | Diabetes Mellitus, Experimental - complications | Antirheumatic Agents - pharmacology | Interleukin 1 Receptor Antagonist Protein - pharmacology | Diabetes Mellitus, Experimental - metabolism | Macrophages - immunology | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism | Arrhythmias, Cardiac - metabolism | Myocardial Contraction | Receptors, Interleukin-1 - immunology | NLR Family, Pyrin Domain-Containing 3 Protein - antagonists & inhibitors | Tachycardia, Ventricular - etiology | Interleukin-1beta - immunology | Mice, Transgenic | Arrhythmias, Cardiac - etiology | Diabetes Mellitus, Experimental - immunology | Animals | NLR Family, Pyrin Domain-Containing 3 Protein - immunology | Myocytes, Cardiac - metabolism | Toll-Like Receptor 2 - immunology | Mice | Receptors, Interleukin-1 - antagonists & inhibitors | Tachycardia, Ventricular - immunology
Journal Article
Circulation Research, ISSN 0009-7330, 09/2015, Volume 117, Issue 8, pp. 720 - 730
RATIONALE:Tissue engineering approaches may improve survival and functional benefits from human embryonic stem cell–derived cardiomyocyte transplantation,... 
Myocardial infarction | Cell survival | Cardiac function tests | Tissue engineering | Myocardial ischemia | Transplantation | Cardiac MRI | tissue engineering | cell survival | cardiac MRI | myocardial infarction | transplantation | myocardial ischemia | cardiac function tests | CARDIAC & CARDIOVASCULAR SYSTEMS | TISSUE | CARDIOMYOPATHY | CELL-DERIVED CARDIOMYOCYTES | COCULTURE | SHEETS | CARDIAC RHABDOMYOMA | RAT HEARTS | REPAIR | EMBRYONIC STEM-CELLS | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | Embryonic Stem Cells - metabolism | Myocytes, Cardiac - immunology | Humans | Male | Papillary Muscles - transplantation | Rats, Nude | Myocardial Infarction - immunology | Heterografts | Transfection | Time Factors | Myocardial Infarction - pathology | Myocardial Infarction - physiopathology | Papillary Muscles - metabolism | Cell Differentiation | Embryonic Stem Cells - immunology | Immunosuppressive Agents - pharmacology | Disease Models, Animal | Biomarkers - metabolism | Myocardial Contraction | Myocardial Infarction - surgery | Cell Line | Tissue Engineering - methods | Connexin 43 - metabolism | Papillary Muscles - immunology | Cell Survival | Heart Transplantation - adverse effects | Graft Survival | Myocardial Infarction - metabolism | Rats, Sprague-Dawley | Stroke Volume | Myocytes, Cardiac - pathology | Myocytes, Cardiac - transplantation | Papillary Muscles - physiopathology | Animals | Heart Transplantation - methods | Embryonic Stem Cells - transplantation | Myocytes, Cardiac - metabolism | Papillary Muscles - pathology | Index Medicus | Human embryonic stem cells | engineered heart muscle | cardiac magnetic resonance imaging | cardiac function
Journal Article
Journal of Molecular and Cellular Cardiology, ISSN 0022-2828, 2016, Volume 91, pp. 123 - 133
Abstract CD4+ T cell activation plays a key role in facilitating wound healing after myocardial infarction (MI). Exosomes (EXs) secreted from dendritic cells... 
Cardiovascular | Myocardial infarction | T-lymphocytes | Dendritic cells | Cytokines | Exosomes | Chemokines | RESPONSES | CARDIAC & CARDIOVASCULAR SYSTEMS | MIP-1-ALPHA | PRECURSORS | CELL BIOLOGY | Myocardium - immunology | Spleen - immunology | Myocytes, Cardiac - immunology | Dendritic Cells - immunology | Culture Media, Conditioned - pharmacology | Male | Spleen - drug effects | Myocardial Infarction - rehabilitation | Necrosis - pathology | Myocardial Infarction - immunology | Necrosis - immunology | CD4-Positive T-Lymphocytes - immunology | Cell Hypoxia | Myocardial Infarction - therapy | Bone Marrow Cells - immunology | Myocardial Infarction - pathology | Myocardium - metabolism | Exosomes - immunology | Bone Marrow Cells - drug effects | Dendritic Cells - drug effects | Cytokines - genetics | Wound Healing - drug effects | Cytokines - immunology | Disease Models, Animal | Necrosis - rehabilitation | Exosomes - transplantation | Signal Transduction | Bone Marrow Cells - cytology | CD4-Positive T-Lymphocytes - cytology | Mice, Inbred C57BL | Gene Expression Regulation | Myocardium - pathology | Spleen - cytology | Wound Healing - immunology | Myocytes, Cardiac - pathology | Animals | Myocytes, Cardiac - drug effects | Lymphocyte Activation - drug effects | Necrosis - therapy | Dendritic Cells - cytology | Mice | Primary Cell Culture | CD4-Positive T-Lymphocytes - drug effects | Cytokines - biosynthesis | Cell Movement
Journal Article
Cardiovascular research, ISSN 0008-6363, 08/2013, Volume 99, Issue 3, pp. 422 - 431
Journal Article
Nature, ISSN 0028-0836, 2016, Volume 538, Issue 7625, pp. 388 - 391
Journal Article