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Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 8/2013, Volume 110, Issue 34, pp. 13839 - 13844
The adult mammalian heart has limited potential for regeneration. Thus, after injury, cardiomyocytes are permanently lost, and contractility is diminished. In... 
Heart | Regeneration | Transcription factors | Ligation | Alleles | Fibrosis | Myocardium | Photoreceptors | Left coronary artery | Cardiac output | Cardiac fibrosis | Cardiomyopathy | Cell cycle | TRANSCRIPTION FACTORS | F-ACTIN | cell cycle | ORGAN SIZE CONTROL | MULTIDISCIPLINARY SCIENCES | CARDIOMYOCYTE PROLIFERATION | ZEBRAFISH HEART REGENERATION | MIR-15 FAMILY | TEAD/TEF FAMILY | cardiac fibrosis | SIGNALING PATHWAY | IN-VIVO | cardiomyopathy | HOLT-ORAM-SYNDROME | Echocardiography | Heart - physiology | Myocardial Contraction - physiology | Mice, Transgenic | DNA Primers - genetics | Phosphoproteins - genetics | Transcription Factors - genetics | Phosphoproteins - metabolism | Regeneration - physiology | Blotting, Western | Mutation, Missense - genetics | Tetrazolium Salts | Transcription Factors - metabolism | Myocardial Contraction - genetics | Animals | Histological Techniques | Myocytes, Cardiac - physiology | Adaptor Proteins, Signal Transducing - genetics | Myocytes, Cardiac - metabolism | Signal Transduction - physiology | Mice | Adaptor Proteins, Signal Transducing - metabolism | Protein-Serine-Threonine Kinases - metabolism | Proteins | Molecular genetics | Heart cells | Cellular control mechanisms | Physiological aspects | Genetic aspects | Regeneration (Biology) | Research | Signal transduction | Tissue engineering | Rodents | Cardiomyocytes | Insulin-like growth factors | Index Medicus | Biological Sciences
Journal Article
Journal of the American College of Cardiology, ISSN 0735-1097, 2012, Volume 60, Issue 2, pp. 144 - 156
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 5/2009, Volume 106, Issue 18, pp. 7636 - 7641
Journal Article
BBA - Molecular Basis of Disease, ISSN 0925-4439, 06/2013, Volume 1832, Issue 6, pp. 848 - 863
Sepsis is characterized by systematic inflammation and contributes to cardiac dysfunction. This study was designed to examine the effect of protein kinase B... 
Heart | ER stress | Sepsis | Akt | Contractile function | Apoptosis | OXIDATIVE STRESS | CONTRACTILE DYSFUNCTION | BIOCHEMISTRY & MOLECULAR BIOLOGY | HEART-FAILURE | ENDOPLASMIC-RETICULUM STRESS | AUTOPHAGY | GROWTH-FACTOR I | SIGNAL-TRANSDUCTION | SYNTHASE | BIOPHYSICS | INFLAMMATORY RESPONSE | NF-KAPPA-B | Caspase 9 - genetics | Apoptosis - drug effects | Calcium - metabolism | Heat-Shock Proteins - biosynthesis | Myocardial Contraction - drug effects | bcl-2-Associated X Protein - biosynthesis | Apoptosis - genetics | Glycogen Synthase Kinase 3 beta | Heat-Shock Proteins - genetics | Phosphorylation - genetics | Caspase 3 - genetics | Phosphorylation - drug effects | Transcription Factor CHOP - biosynthesis | Proto-Oncogene Proteins c-akt - metabolism | Apoptosis Regulatory Proteins - biosynthesis | Lipopolysaccharides - toxicity | Endoplasmic Reticulum Stress - drug effects | Mice, Transgenic | Glycogen Synthase Kinase 3 - genetics | Eukaryotic Initiation Factor-2 - genetics | Mice | Enzyme Activation - genetics | Transcription Factor CHOP - genetics | Eukaryotic Initiation Factor-2 - biosynthesis | Microtubule-Associated Proteins - genetics | bcl-X Protein - genetics | Extracellular Signal-Regulated MAP Kinases - metabolism | Endoplasmic Reticulum Stress - genetics | Extracellular Signal-Regulated MAP Kinases - genetics | Proto-Oncogene Proteins c-akt - genetics | Myocardial Contraction - genetics | MAP Kinase Signaling System - genetics | Apoptosis Regulatory Proteins - genetics | Caspase 3 - biosynthesis | bcl-X Protein - biosynthesis | bcl-2-Associated X Protein - genetics | Beclin-1 | Gene Expression Regulation - genetics | Myocardium - pathology | Transcription Factors - biosynthesis | Transcription Factors - genetics | Enzyme Activation - drug effects | Glycogen Synthase Kinase 3 - metabolism | Microtubule-Associated Proteins - biosynthesis | Gene Expression Regulation - drug effects | Autophagy-Related Protein 7 | Myocardium - enzymology | Animals | MAP Kinase Signaling System - drug effects | Caspase 9 - biosynthesis
Journal Article
Journal Article
Journal of Endocrinology, ISSN 0022-0795, 2017, Volume 232, Issue 3, pp. 437 - 450
Corticosteroids directly affect the heart and vasculature and are implicated in the pathogenesis of heart failure. Attention is focussed upon the role of the... 
Heart | Isovolumetric contraction | Mineralocorticoid receptor | Fibrosis | Glucocorticoid receptor | glucocorticoid receptor | PRESSURE-OVERLOAD | FETAL HEART MATURATION | mineralocorticoid receptor | heart | INDUCED HYPERTENSION | SMOOTH-MUSCLE | DISEASE | ENDOCRINOLOGY & METABOLISM | fibrosis | ALDOSTERONE | MICE | isovolumetric contraction | GENDER-DIFFERENCES | EXPRESSION | Nonmuscle Myosin Type IIB - metabolism | Muscle, Smooth, Vascular - metabolism | Ventricular Function, Left - genetics | Myosin Heavy Chains - genetics | Male | Receptors, Glucocorticoid - metabolism | Fibrosis - metabolism | Myosin Heavy Chains - metabolism | Myocardial Contraction - genetics | Spironolactone - pharmacology | Myocardium - metabolism | Female | Corticosterone - blood | Muscle, Smooth, Vascular - drug effects | Nonmuscle Myosin Type IIB - genetics | Myocardium - pathology | Mice, Knockout | Myocytes, Cardiac - pathology | Muscle, Smooth, Vascular - pathology | Animals | Myocytes, Cardiac - drug effects | Receptors, Glucocorticoid - genetics | Sex Factors | Myocytes, Cardiac - metabolism | Mice | Fibrosis - pathology | Corticoids | Mitral valve | Glucocorticoids | Weaning | Cardiomyocytes | Smooth muscle | Gene expression | Muscle contraction | Contraction | Blood flow | Clonal deletion | Myosin | Ventricle | Heart diseases | Hypertrophy | Index Medicus
Journal Article
Circulation, ISSN 0009-7322, 2011, Volume 123, Issue 9, pp. 979 - 988
Background- Excitation-contraction coupling in striated muscle requires proper communication of plasmalemmal voltage-activated Ca(2+) channels and Ca(2+)... 
heart failure | calcium | junctophilin | excitation | sarcoplasmic reticulum | RNA INTERFERENCE | PRESSURE-OVERLOAD | CARDIAC & CARDIOVASCULAR SYSTEMS | CA2+ RELEASE UNITS | HEART-FAILURE | HYPERTROPHIC CARDIOMYOPATHY | CONTRACTION | CHANNEL | CARDIAC-HYPERTROPHY | PERIPHERAL VASCULAR DISEASE | DYSFUNCTION | SKELETAL | HEMATOLOGY | RNA, Small Interfering - genetics | Calcium Channels - secretion | Membrane Proteins - genetics | Intercellular Junctions - metabolism | Heart Failure - genetics | Mice, Transgenic | Ryanodine Receptor Calcium Release Channel - metabolism | Ryanodine Receptor Calcium Release Channel - ultrastructure | Cell Membrane - genetics | Cell Membrane - ultrastructure | Heart Failure - pathology | Intercellular Junctions - genetics | Gene Knockdown Techniques - methods | Mice, Knockout | Membrane Proteins - deficiency | Myocardial Contraction - genetics | Animals | Ryanodine Receptor Calcium Release Channel - genetics | Cell Membrane - metabolism | Mice | Intercellular Junctions - ultrastructure | Calcium Channels - genetics | Calcium Channels - deficiency | Heart Failure - mortality | Junctional complexes (Epithelium) | Heart failure | Calcium channels | Sarcoplasmic reticulum | Physiological aspects | Cell junctions | Genetic aspects | Models | Research | Risk factors | Index Medicus | Abridged Index Medicus
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 12/2011, Volume 121, Issue 12, pp. 4640 - 4654
Human mutations in or variants of TBX20 are associated with congenital heart disease, cardiomyopathy, and arrhythmias. To investigate whether cardiac disease... 
MEDICINE, RESEARCH & EXPERIMENTAL | SEVERE FORM | TRANSCRIPTION FACTOR TBX20 | CONGENITAL HEART-DISEASE | EMBRYONIC LETHALITY | NKX2.5 MUTATIONS | DILATED CARDIOMYOPATHY | HOLT-ORAM-SYNDROME | TARGETED DELETION | EXPRESSION | MICE LACKING | T-Box Domain Proteins - physiology | Rats, Wistar | Cytoskeletal Proteins - genetics | Humans | Myocardial Contraction - physiology | Heart Failure - physiopathology | Ion Channels - genetics | Male | Zebrafish - embryology | Arrhythmias, Cardiac - physiopathology | Arrhythmias, Cardiac - pathology | Cardiomyopathies - genetics | Cardiomyopathies - physiopathology | Myocardial Contraction - genetics | Chromatin Immunoprecipitation | Cytoskeletal Proteins - biosynthesis | Binding Sites | Heart Failure - etiology | Arrhythmias, Cardiac - genetics | Genes, Reporter | Ion Channels - biosynthesis | T-Box Domain Proteins - deficiency | Animals, Genetically Modified | Gene Expression Regulation - genetics | Heart - growth & development | Rats | Cardiomyopathies - pathology | Heart Failure - genetics | Transcription Factors - biosynthesis | Arrhythmias, Cardiac - etiology | Heart Failure - pathology | Transcription Factors - genetics | T-Box Domain Proteins - genetics | Mice, Knockout | Gene Expression Regulation - drug effects | Myocardial Infarction - complications | Animals | Myocytes, Cardiac - physiology | Mice | Ion Transport - genetics | Transcription factors | Heart cells | Genetic aspects | Research | Genetic regulation | Properties | Gene expression | Index Medicus | Abridged Index Medicus
Journal Article
Circulation Research, ISSN 0009-7330, 09/2008, Volume 103, Issue 6, pp. 580 - 590
Journal Article
Basic Research in Cardiology, ISSN 0300-8428, 5/2013, Volume 108, Issue 3, pp. 1 - 12
Hypertrophic cardiomyopathy (HCM) is a myocardial disease associated with mutations in sarcomeric genes. Three mutations were found in ANKRD1, encoding ankyrin... 
ANKRD1 | Hypertrophic cardiomyopathy | Medicine & Public Health | Cardiology | Sarcomere | Engineered heart tissue | CARDIAC & CARDIOVASCULAR SYSTEMS | ANKYRIN REPEAT PROTEIN | CARP | MYOCYTES | STRESS-RESPONSE | DILATED CARDIOMYOPATHY | SKELETAL-MUSCLE | DISEASE | GENE-EXPRESSION | DYSFUNCTION | MOLECULAR-BASIS | Dependovirus - genetics | Humans | Myocardial Contraction - drug effects | Green Fluorescent Proteins - genetics | Myocardial Contraction - genetics | Transfection | Time Factors | Muscle Proteins - metabolism | Nuclear Proteins - genetics | Repressor Proteins - metabolism | Animals, Newborn | Green Fluorescent Proteins - metabolism | Cardiomyopathy, Hypertrophic - genetics | Tissue Engineering - methods | Transduction, Genetic | Proteasome Inhibitors - pharmacology | Cardiomyopathy, Hypertrophic - metabolism | Cells, Cultured | Gene Expression Regulation | Rats | Repressor Proteins - genetics | Genotype | Nuclear Proteins - metabolism | Muscle Proteins - genetics | Phenotype | Animals | Myocytes, Cardiac - drug effects | Cardiomyopathy, Hypertrophic - physiopathology | Fluorescent Antibody Technique | Myocytes, Cardiac - metabolism | Mutation | Proteasome Endopeptidase Complex - metabolism | Genetic Vectors | Oligopeptides - pharmacology | Genetic aspects | Cardiomyopathy, Hypertrophic | Universities and colleges | Analysis | Index Medicus
Journal Article
PLoS Genetics, ISSN 1553-7390, 08/2014, Volume 10, Issue 8, pp. e1004550 - e1004550
Journal Article