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Journal of Molecular and Cellular Cardiology, ISSN 0022-2828, 2013, Volume 65, pp. 108 - 119
Journal Article
PloS one, ISSN 1932-6203, 2013, Volume 8, Issue 9, pp. e74535 - e74535
Senescence is a recognized mechanism of cardiovascular diseases; however, its contribution to myocardial fibrosis and rupture after infarction and the... 
APOPTOSIS | PREMATURE SENESCENCE | MULTIDISCIPLINARY SCIENCES | VASCULAR CELL SENESCENCE | PHENOTYPE | TUMOR-SUPPRESSOR | MICE | MODEL | INFLAMMATORY RESPONSE | P53 | DELETION | Myocardial Infarction - genetics | RNA, Small Interfering - genetics | Adenoviridae | Endomyocardial Fibrosis - etiology | Tumor Suppressor Protein p53 - antagonists & inhibitors | Male | Tumor Suppressor Protein p53 - genetics | Myocardial Infarction - pathology | Myocardium - metabolism | Endomyocardial Fibrosis - genetics | Collagen - genetics | Endomyocardial Fibrosis - pathology | Disease Models, Animal | Fibroblasts - metabolism | Cellular Senescence - genetics | Signal Transduction | Cells, Cultured | Gene Expression Regulation | Myocardium - pathology | Myocardial Infarction - metabolism | Fibroblasts - pathology | Tumor Suppressor Protein p53 - deficiency | Mice, Knockout | Collagen - metabolism | Myocardial Infarction - complications | Animals | Endomyocardial Fibrosis - metabolism | Mice | Cell Hypoxia - genetics | Genetic Vectors | Cell Movement | RNA, Small Interfering - metabolism | Heart | Collagen | Adenoviruses | Fibrosis | Tumor proteins | Health aspects | Heart attack | Myocardial infarction | Regulators | Senescence | Immunoglobulins | Matrix metalloproteinases | Heart attacks | p53 Protein | Rupture | siRNA | Macrophages | Genotype & phenotype | Hospitals | Education | Fibroblasts | Hypoxia | Infiltration | Infarction | Diabetes | Laboratory animals | Cardiovascular diseases | Heart diseases | Index Medicus
Journal Article
PLoS ONE, ISSN 1932-6203, 11/2016, Volume 11, Issue 11, pp. e0166480 - e0166480
Cytokine-like 1 (Cytl1) is a secreted protein that is involved in diverse biological processes. A comparative modeling study indicated that Cytl1 is... 
FIBROBLAST PRECURSORS | MOLECULAR-CLONING | EXPRESSION | MULTIDISCIPLINARY SCIENCES | MYOFIBROBLAST | GROWTH | Receptors, CCR2 - genetics | Myocardial Infarction - genetics | Receptors, Transforming Growth Factor beta - genetics | Transforming Growth Factor beta2 - metabolism | Humans | Male | Myofibroblasts - metabolism | Myocardial Reperfusion Injury - pathology | Cell Transdifferentiation - drug effects | Myocardial Infarction - pathology | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Dioxoles - pharmacology | Endomyocardial Fibrosis - genetics | Benzamides - pharmacology | Endomyocardial Fibrosis - pathology | Receptors, Cytokine - metabolism | Myocardial Reperfusion Injury - genetics | Receptors, Cytokine - genetics | Protein-Serine-Threonine Kinases - metabolism | Disease Models, Animal | Fibroblasts - metabolism | Myofibroblasts - pathology | Signal Transduction | Gene Expression Regulation | Protein-Serine-Threonine Kinases - genetics | Heart Failure - genetics | Smad Proteins - genetics | Heart Failure - metabolism | Heart Failure - pathology | Myocardial Infarction - metabolism | Fibroblasts - pathology | Myofibroblasts - drug effects | Mice, Knockout | Myocardial Reperfusion Injury - metabolism | Receptors, CCR2 - metabolism | Animals | Constriction, Pathologic - surgery | Receptors, Transforming Growth Factor beta - antagonists & inhibitors | Receptors, Transforming Growth Factor beta - metabolism | Aorta - surgery | Fibroblasts - drug effects | Endomyocardial Fibrosis - metabolism | Mice | Transforming Growth Factor beta2 - genetics | Smad Proteins - metabolism | Heart | CC chemokine receptors | Smad protein | Heart attacks | Mesenchyme | Viruses | Kinases | Proteins | Signal transduction | CCR2 protein | Ischemia | Rodents | Fibroblasts | Life sciences | Heart diseases | Carbon-carbon composites | Cytokines | Cloning | Cardiomyocytes | Biological activity | Medicine | Signaling | Ostomy | Monocyte chemoattractant protein | Coronary vessels | Fibrosis | Chemokines | Monocyte chemoattractant protein 1 | Veins & arteries | Index Medicus
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 09/2014, Volume 289, Issue 39, pp. 27199 - 27214
Journal Article
PLoS ONE, ISSN 1932-6203, 08/2014, Volume 9, Issue 8, pp. e103793 - e103793
Atrial hypertrophy and fibrosis are essential pathological features of atrial fibrillation. Recently, adiponectin has become a protein of interest due to its... 
FIBRILLATION | HEART | ACTIVATED PROTEIN-KINASE | MULTIDISCIPLINARY SCIENCES | MECHANISMS | DEATH | AKT | VASCULAR ENDOTHELIAL-CELLS | KAPPA-B | CARDIOMYOCYTES | RECEPTORS | AMP-Activated Protein Kinases - metabolism | Heart Atria - pathology | Receptors, Adiponectin - metabolism | Cardiomegaly - pathology | NF-kappa B - metabolism | Phosphatidylinositol 3-Kinases - metabolism | Adiponectin - metabolism | Endomyocardial Fibrosis - chemically induced | Endomyocardial Fibrosis - pathology | Angiotensin II - adverse effects | Fibroblasts - metabolism | Vasoconstrictor Agents - pharmacology | Endomyocardial Fibrosis - prevention & control | Angiotensin II - pharmacology | Vasoconstrictor Agents - adverse effects | Rats | Fibroblasts - pathology | Rats, Sprague-Dawley | Heart Atria - metabolism | Nerve Tissue Proteins - metabolism | Myocytes, Cardiac - pathology | Animals | Cardiomegaly - prevention & control | Signal Transduction - drug effects | Cardiomegaly - chemically induced | Endomyocardial Fibrosis - metabolism | Myocytes, Cardiac - metabolism | Adaptor Proteins, Signal Transducing - metabolism | Cardiomegaly - metabolism | Infection | Heart | RNA | Heart enlargement | Atrial fibrillation | Fibrosis | Angiotensin | Natriuretic peptides | Neonates | AKT protein | Myocytes | Proteins | Angiogenesis | Signal transduction | Fibrillation | Ischemia | Penicillin | Fibroblasts | Inhibition | Medical research | NF-κB protein | Cytokines | AMP | Metabolism | Gene expression | Insulin | 1-Phosphatidylinositol 3-kinase | Hospitals | Molecular modelling | Cardiovascular diseases | Fluorescence microscopy | Hypertrophy | Biotechnology | Phosphorylation | Laboratories | Fluorescence | Atrial natriuretic peptide | Kinases | Western blotting | Adiponectin | Engineering | Pathways | Rodents | Atherosclerosis | Angiotensin II | Cardiology | Heart diseases | Translocation | Procollagen | Adenosine monophosphate | Therapeutic applications | Cardiomyocytes | Medicine | Signaling | Protein kinase | Adenosine kinase | Pharmaceuticals | Index Medicus
Journal Article
Circulation, ISSN 0009-7322, 09/2004, Volume 110, Issue 10, pp. 1263 - 1268
Journal Article
Journal Article
PLoS ONE, ISSN 1932-6203, 04/2015, Volume 10, Issue 4, pp. e0125513 - e0125513
MicroRNA-7a/b (miR-7a/b) protects cardiac myocytes from apoptosis during ischemia/reperfusion injury; however, its role in angiotensin II (ANG II)-stimulated... 
CELLS | ACTIVATION | COLLAGEN GENE | MULTIDISCIPLINARY SCIENCES | TRANSCRIPTION | DOWN-REGULATION | NECROSIS-FACTOR-ALPHA | PROLIFERATION | NF-KAPPA-B | MATRIX GENE-EXPRESSION | DNA-BINDING ACTIVITY | Angiotensin II - pharmacology | Matrix Metalloproteinase 9 - biosynthesis | Rats, Wistar | Rats | MicroRNAs - biosynthesis | Myocardium - pathology | Sp1 Transcription Factor - metabolism | Extracellular Signal-Regulated MAP Kinases - metabolism | Fibroblasts - pathology | Plicamycin - pharmacology | Gene Expression Regulation - drug effects | Cell Movement - drug effects | Collagen Type I - biosynthesis | Animals | MAP Kinase Signaling System - drug effects | Myocardium - metabolism | Endomyocardial Fibrosis - metabolism | Endomyocardial Fibrosis - chemically induced | Endomyocardial Fibrosis - pathology | Angiotensin II - adverse effects | Transforming Growth Factor beta - metabolism | Matrix Metalloproteinase 2 - biosynthesis | Fibroblasts - metabolism | Heart | Collagen (type I) | Phosphorylation | Migration | Activation | Myocytes | Kinases | Proteins | Reperfusion | Pathways | Ischemia | Education | Rodents | Cell cycle | Fibroblasts | Extracellular matrix | Tumor necrosis factor-TNF | Physiology | Inhibition | Angiotensin II | Cardiology | Growth factors | Heart diseases | Public health | Hypertension | MiRNA | Extracellular signal-regulated kinase | Cardiomyocytes | JNK protein | Gene expression | Sp1 protein | Ribonucleic acid--RNA | Gelatinase B | Gelatinase A | Hospitals | Collagen | Fibrosis | Angiotensin | Laboratory animals | Molecular biology | Apoptosis | Index Medicus | RNA | Ribonucleic acid
Journal Article
PLoS ONE, ISSN 1932-6203, 04/2012, Volume 7, Issue 4, pp. e35905 - e35905
Hematopoietic progenitor CD133(+)/c-kit(+) cells have been shown to be involved in myocardial healing following myocardial infarction (MI). Previously we... 
CD31(+) CELLS | ENDOTHELIAL PROGENITOR CELLS | ISCHEMIA/REPERFUSION INJURY | ACTIVATION | ISCHEMIC VASCULAR-DISEASE | ANGIOGENIC ACTIVITY | BONE-MARROW | BIOLOGY | RECEPTOR | TOPCARE-AMI | EXPRESSION | Up-Regulation | Capillaries - pathology | Receptors, Notch - metabolism | Cardiomegaly - pathology | Angiopoietin-1 - metabolism | Antigens, CD - metabolism | Peptides - metabolism | Serrate-Jagged Proteins | Bone Marrow - metabolism | Myocardium - metabolism | Endomyocardial Fibrosis - complications | Myocardial Infarction - physiopathology | Capillaries - metabolism | Apelin | Jagged-1 Protein | Capillaries - physiopathology | Signal Transduction | Cardiomegaly - physiopathology | Myocardial Infarction - metabolism | Receptors, CXCR4 - metabolism | Chemokine CXCL12 - metabolism | Hematopoietic Stem Cells - cytology | Endomyocardial Fibrosis - metabolism | Mice | Diabetes Mellitus, Type 2 - pathology | Cardiomegaly - metabolism | Cell Movement | Actins - metabolism | Glycoproteins - metabolism | Diabetes Mellitus, Type 2 - metabolism | Proto-Oncogene Proteins c-kit - metabolism | Intercellular Signaling Peptides and Proteins - metabolism | Platelet Endothelial Cell Adhesion Molecule-1 - metabolism | Myocardial Infarction - pathology | Endomyocardial Fibrosis - pathology | Membrane Proteins - metabolism | Heart Function Tests | Diabetes Mellitus, Type 2 - complications | Calcium-Binding Proteins - metabolism | Myocardium - pathology | Adipokines | AC133 Antigen | Cardiomegaly - complications | Myocardial Infarction - complications | Animals | Diabetes Mellitus, Type 2 - physiopathology | Bone Marrow - pathology | Receptor, Notch3 | Endomyocardial Fibrosis - physiopathology | Apoptosis | Advertising executives | Vascular endothelial growth factor | Adenoviruses | Heart attack | Myocardial infarction | Heart | Diabetic retinopathy | Heart attacks | Angiopoietin | Recovery of function | Smooth muscle | Cardiovascular disease | Recruitment | Angiogenesis | Toxicology | Cell growth | Ischemia | Data recovery | Rodents | Bone marrow | Repair | Heart diseases | Immunoglobulins | Diabetes mellitus | Coronary artery | Muscles | Pharmacology | c-Kit protein | Hemopoiesis | Studies | Ostomy | Coronary vessels | Fibrosis | Stem cells | Myocardium | Infarction | Diabetes | Laboratory animals | Index Medicus
Journal Article
Journal Article
Biochemical Journal, ISSN 0264-6021, 02/2017, Volume 474, Issue 3, pp. 399 - 410
Cardiac fibrosis and chronic inflammation are common complications in type 2 diabetes mellitus (T2D). Since nucleotide oligomerization-binding domain 1 (NOD1),... 
PLASMINOGEN-ACTIVATOR | INSULIN-RESISTANCE | BIOCHEMISTRY & MOLECULAR BIOLOGY | IN-VIVO | DISEASE | TOLL-LIKE RECEPTORS | HOST-DEFENSE | FACTOR-KAPPA-B | EXPRESSION | INNATE IMMUNITY | ADIPOSE-TISSUE | NIH 3T3 Cells | Diaminopimelic Acid - pharmacology | Nitriles - pharmacology | Diabetes Mellitus, Type 2 - genetics | Humans | Nod1 Signaling Adaptor Protein - agonists | Diabetes Mellitus, Experimental - genetics | NF-kappa B - metabolism | Diabetes Mellitus, Type 2 - metabolism | Insulin - blood | Sulfones - pharmacology | Nod1 Signaling Adaptor Protein - metabolism | Transforming Growth Factor beta - agonists | Myocardium - metabolism | Endomyocardial Fibrosis - genetics | Endomyocardial Fibrosis - pathology | Diabetes Mellitus, Experimental - metabolism | Endomyocardial Fibrosis - prevention & control | NF-kappa B - antagonists & inhibitors | Signal Transduction | Gene Expression Regulation | Insulin Resistance | Mice, Transgenic | Myocardium - pathology | Animals | Transforming Growth Factor beta - genetics | Diaminopimelic Acid - analogs & derivatives | NF-kappa B - genetics | Diabetes Mellitus, Experimental - pathology | Endomyocardial Fibrosis - metabolism | Mice | Diabetes Mellitus, Type 2 - pathology | Blood Glucose - metabolism | Transforming Growth Factor beta - metabolism | Nod1 Signaling Adaptor Protein - genetics | Index Medicus
Journal Article
Peptides, ISSN 0196-9781, 02/2016, Volume 76, pp. 108 - 114
Journal Article