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Journal of Molecular and Cellular Cardiology, ISSN 0022-2828, 2014, Volume 72, pp. 296 - 304
Abstract Background Cardiomyocytes derived from human induced pluripotent stem cells (hiPSC-CMs) have great potential as a cell source for therapeutic... 
Cardiovascular | Cardiomyocyte maturation | Mitochondria | Tri-iodo-l-thyronine | Human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) | Contractile force | CARDIAC & CARDIOVASCULAR SYSTEMS | FUNCTIONAL MATURATION | THYROID-HORMONE | SIZE | LINES | CELL BIOLOGY | PASSIVE STIFFNESS | CARDIAC-HYPERTROPHY | FETAL | DIFFERENTIATION | SECRETION | Tri-iodo-L-thyronine | UP-REGULATION | Calcium - metabolism | Humans | Culture Media, Conditioned - pharmacology | Lung - cytology | Oxidative Phosphorylation - drug effects | Cyclin-Dependent Kinase Inhibitor p21 - genetics | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Lung - metabolism | Induced Pluripotent Stem Cells - cytology | Fibroblasts - metabolism | Induced Pluripotent Stem Cells - metabolism | Triiodothyronine - pharmacology | Gene Expression | Sarcoplasmic Reticulum Calcium-Transporting ATPases - metabolism | Induced Pluripotent Stem Cells - drug effects | Myocytes, Cardiac - cytology | Sarcomeres - drug effects | Sarcomeres - metabolism | Cells, Cultured | Mitochondria - metabolism | Mitochondria - drug effects | Animals | Myocytes, Cardiac - drug effects | Cell Differentiation - drug effects | Fibroblasts - drug effects | Lung - drug effects | Myocytes, Cardiac - metabolism | Fibroblasts - cytology | Mice | Cell Cycle - drug effects | Sarcoplasmic Reticulum Calcium-Transporting ATPases - genetics | Analysis | Stem cells | Heart cells | Index Medicus | Human induced pluripotent stem cells-derived cardiomyocytes (hiPSC-CMs)
Journal Article
Journal Article
Journal Article
Biomaterials, ISSN 0142-9612, 2015, Volume 70, pp. 94 - 104
Abstract Generation of de novo cardiomyocytes through viral over-expression of key transcription factors represents a highly promising strategy for cardiac... 
Advanced Basic Science | Dentistry | Micropatterning | Surface topography | Stem cell | Cardiomyocyte | Cardiac tissue engineering | MOUSE FIBROBLASTS | STEM-CELLS | MEF2C | MATERIALS SCIENCE, BIOMATERIALS | ENGINEERING, BIOMEDICAL | GATA4 | INDUCTION | CELL-SHAPE | BIOPHYSICAL REGULATION | HISTONE ACETYLATION | DIFFERENTIATE | SUMOYLATION | Myocytes, Cardiac - cytology | Sarcomeres - drug effects | Sarcomeres - metabolism | Nuclear Proteins - metabolism | Side-Population Cells - cytology | Cell Lineage - drug effects | Valproic Acid - pharmacology | Side-Population Cells - drug effects | Sumoylation - drug effects | Cellular Reprogramming - drug effects | Acetylation - drug effects | Cell Nucleus - metabolism | Dimethylpolysiloxanes - pharmacology | Myocytes, Cardiac - drug effects | Myocytes, Cardiac - metabolism | Trans-Activators - metabolism | Clone Cells | Dimethylpolysiloxanes - chemistry | Histones - metabolism | Cell Nucleus - drug effects | Cellular Reprogramming - genetics | Real-Time Polymerase Chain Reaction | Proteins | Post-translational modification | Heart | Divalproex | Anisotropy | Genetically modified organisms | Genetic research | Genetic engineering | Valproic acid | Biomedical engineering | Tissue engineering | DNA binding proteins | Cues | Surgical implants | Biomedical materials | Cellular | Histones | Strategy | Genetic algorithms
Journal Article
Journal Article
American Journal of Physiology - Heart and Circulatory Physiology, ISSN 0363-6135, 2015, Volume 309, Issue 10, pp. H1720 - H1730
S-glutathionylation of cardiac myosin-binding protein C (cMyBP-C) induces Ca2+ sensitization and a slowing of cross-bridge kinetics as a result of increased... 
Oxidative stress | Diastolic dysfunction | Cardiac myosin-binding protein C | S-glutathionylation | Sarcomeres | BINDING-PROTEIN-C | MYOFILAMENT RESPONSE | CARDIAC & CARDIOVASCULAR SYSTEMS | PHYSIOLOGY | sarcomeres | TROPONIN-I | CA2 | RECOMMENDATIONS | cardiac myosin-binding protein C | CARDIAC-HYPERTROPHY | MUTATION | diastolic dysfunction | PERIPHERAL VASCULAR DISEASE | ECHOCARDIOGRAPHY | oxidative stress | ALPHA-TROPOMYOSIN | Free Radical Scavengers - pharmacology | Tropomyosin - genetics | Calcium - metabolism | Cardiomyopathy, Hypertrophic, Familial - genetics | Calcium-Binding Proteins - drug effects | Male | Mitogen-Activated Protein Kinase 1 - drug effects | Carrier Proteins - drug effects | Sarcoplasmic Reticulum Calcium-Transporting ATPases - drug effects | Mitogen-Activated Protein Kinase 3 - drug effects | Female | Diastole - drug effects | Phosphorylation - drug effects | Disease Models, Animal | Calcium-Binding Proteins - metabolism | Cardiomyopathy, Hypertrophic, Familial - physiopathology | Myofibrils - drug effects | Sarcoplasmic Reticulum Calcium-Transporting ATPases - metabolism | Cardiomyopathy, Hypertrophic, Familial - metabolism | Mice, Transgenic | Animals | Carrier Proteins - metabolism | Heart Ventricles - physiopathology | Mitogen-Activated Protein Kinase 3 - metabolism | Acetylcysteine - pharmacology | Heart Ventricles - metabolism | Mice | Myofibrils - metabolism | Oxidative Stress - drug effects | Heart Ventricles - drug effects | Mitogen-Activated Protein Kinase 1 - metabolism | Complications and side effects | Care and treatment | Usage | Cardiomyopathy, Hypertrophic | Analysis | Acetylcysteine | Protein C | Influence | Genetic aspects | Genetic engineering | Research | Hypertrophy | Muscle Mechanics and Ventricular Function
Journal Article
SCIENCE, ISSN 0036-8075, 02/2016, Volume 351, Issue 6273, pp. 617 - 621
Journal Article
Journal Article
Circulation, ISSN 0009-7322, 12/2011, Volume 124, Issue 25, pp. 2882 - 2891
Background-In vitro studies suggest that phosphorylation of titin reduces myocyte/myofiber stiffness. Titin can be phosphorylated by cGMP-activated protein... 
Cyclic GMP-dependent protein kinases | Sildenafil | brain | Natriuretic peptide | Heart failure, diastolic | heart failure, diastolic | CARDIAC & CARDIOVASCULAR SYSTEMS | HEART-FAILURE | PROTEIN-KINASE-I | cyclic GMP-dependent protein kinases | RELAXATION | PRESERVED EJECTION FRACTION | DILATED CARDIOMYOPATHY | sildenafil | RAT CARDIAC MYOCYTES | PASSIVE STIFFNESS | NITRIC-OXIDE | PERIPHERAL VASCULAR DISEASE | HEMODYNAMIC-RESPONSES | natriuretic peptide, brain | LEFT-VENTRICULAR FUNCTION | Protein Kinases - metabolism | Connectin | Age Factors | Hypertension - drug therapy | Natriuretic Peptide, Brain - pharmacology | Sulfones - pharmacology | Sildenafil Citrate | Compliance - drug effects | Ventricular Pressure - physiology | Muscle Proteins - metabolism | Ventricular Function, Left - physiology | Diastole - drug effects | Phosphorylation - drug effects | Vasodilator Agents - pharmacology | Purines - pharmacology | Sarcomeres - metabolism | Ventricular Function, Left - drug effects | Ventricular Pressure - drug effects | Diastole - physiology | Piperazines - pharmacology | Hypertension - pathology | Hypertension - physiopathology | Myocytes, Cardiac - pathology | Animals | Myocytes, Cardiac - drug effects | Aging - physiology | Cyclic GMP - metabolism | Biopsy | Myocytes, Cardiac - physiology | Dogs | Heart failure | Care and treatment | Patient outcomes | Dosage and administration | Research | Protein kinases | Natriuretic peptides
Journal Article
American Journal of Physiology - Heart and Circulatory Physiology, ISSN 0363-6135, 2015, Volume 308, Issue 9, pp. H1126 - H1135
Overnutrition/obesity predisposes individuals, particularly women, to diastolic dysfunction (DD), an independent predictor of future cardiovascular disease. We... 
Oxidative stress | Low-dose spironolactone | High-fat diet | Cardiac hypertrophy | Mineralocorticoid antagonism | Inflammation | Aldosterone | High-fructose diet | Myocardial compliance | METABOLIC SYNDROME | CARDIAC & CARDIOVASCULAR SYSTEMS | PHYSIOLOGY | aldosterone | HEART-FAILURE | low-dose spironolactone | mineralocorticoid antagonism | PRESERVED EJECTION FRACTION | BLOOD-PRESSURE | DIABETES-MELLITUS | LEFT-VENTRICULAR DYSFUNCTION | inflammation | INSULIN-RESISTANCE | high-fat diet | PERIPHERAL VASCULAR DISEASE | high-fructose diet | CARDIOVASCULAR-DISEASES | cardiac hypertrophy | oxidative stress | myocardial compliance | OBESITY-RELATED CHANGES | Spironolactone - administration & dosage | Receptors, Mineralocorticoid - metabolism | Cardiomegaly - pathology | Heart Ventricles - immunology | Receptors, Mineralocorticoid - drug effects | Ribosomal Protein S6 Kinases, 90-kDa - metabolism | Time Factors | Diet, High-Fat | Inflammation Mediators - metabolism | Ventricular Dysfunction, Left - pathology | Female | Diastole - drug effects | Dietary Sucrose | Diet, Western | Heart Ventricles - pathology | Disease Models, Animal | Mineralocorticoid Receptor Antagonists - administration & dosage | Sarcomeres - drug effects | Sarcomeres - metabolism | Mice, Inbred C57BL | Ventricular Function, Left - drug effects | Ventricular Pressure - drug effects | Cardiomegaly - physiopathology | Ventricular Dysfunction, Left - etiology | Ventricular Dysfunction, Left - immunology | Fructose | Ventricular Dysfunction, Left - physiopathology | Ventricular Dysfunction, Left - prevention & control | Ventricular Dysfunction, Left - metabolism | Animals | Cardiomegaly - prevention & control | Myocytes, Cardiac - drug effects | Heart Ventricles - physiopathology | Fibrosis | Sex Factors | Myocytes, Cardiac - metabolism | Heart Ventricles - metabolism | Oxidative Stress - drug effects | Ventricular Remodeling - drug effects | Heart Ventricles - drug effects | Hypertension | Development and progression | Diet | Spironolactone | Health aspects | Integrative Cardiovascular Physiology and Pathophysiology
Journal Article
Circulation Research, ISSN 0009-7330, 02/2009, Volume 104, Issue 4, pp. e30 - e41
Human induced pluripotent stem (iPS) cells hold great promise for cardiovascular research and therapeutic applications, but the ability of human iPS cells to... 
Action potential | Differentiation | Embryonic stem cells | Induced pluripotent stem cells | Cardiomyocyte | CARDIAC & CARDIOVASCULAR SYSTEMS | differentiation | embryonic stem cells | CARDIAC MYOCYTES | INDUCTION | action potential | LINES | OCT4 | cardiomyocyte | HUMAN FIBROBLASTS | PERIPHERAL VASCULAR DISEASE | induced pluripotent stem cells | GENERATION | HEMATOLOGY | DEVELOP | Embryonic Stem Cells - metabolism | RNA-Binding Proteins - genetics | Cell Proliferation | Homeodomain Proteins - metabolism | Humans | Myocardial Contraction - drug effects | SOXB1 Transcription Factors - metabolism | Action Potentials | Octamer Transcription Factor-3 - genetics | Cell Differentiation - genetics | SOXB1 Transcription Factors - genetics | Time Factors | Cell Line | Nanog Homeobox Protein | Transduction, Genetic | Sarcomeres - metabolism | Pluripotent Stem Cells - physiology | Gene Expression Regulation | Adrenergic beta-Agonists - pharmacology | Embryonic Stem Cells - physiology | Homeodomain Proteins - genetics | Pluripotent Stem Cells - metabolism | Phenotype | Myocytes, Cardiac - drug effects | Embryonic Stem Cells - drug effects | Myocytes, Cardiac - physiology | Isoproterenol - pharmacology | Octamer Transcription Factor-3 - metabolism | Pluripotent Stem Cells - drug effects | Myocytes, Cardiac - metabolism | RNA-Binding Proteins - metabolism
Journal Article
Journal Article
Journal of Molecular and Cellular Cardiology, ISSN 0022-2828, 2015, Volume 94, pp. 95 - 106
Journal Article