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Nature, ISSN 0028-0836, 05/2016, Volume 534, Issue 7605, pp. 119 - 123
Myocardial infarction results in compromised myocardial function and heart failure owing to insufficient cardiomyocyte self-renewal(1). Unlike many... 
RIEGER-SYNDROME | ELEMENTS | OXIDATIVE STRESS | GENE | REGENERATION | MULTIDISCIPLINARY SCIENCES | CARDIOMYOCYTE PROLIFERATION | GROWTH | ENHANCERS | GENOME | FAMILY | Heart Injuries - pathology | Myocardial Infarction - genetics | Protein-Serine-Threonine Kinases - deficiency | Electron Transport - drug effects | Reactive Oxygen Species - metabolism | Antioxidants - metabolism | Electron Transport - genetics | Heart Injuries - metabolism | Homeodomain Proteins - metabolism | Transcription Factors - deficiency | Male | Phosphoproteins - metabolism | Regeneration - genetics | Myocardial Infarction - pathology | Myocardium - metabolism | Female | Wound Healing - genetics | Wound Healing - drug effects | Disease Models, Animal | Animals, Newborn | Heart Injuries - genetics | Free Radical Scavengers - metabolism | Antioxidants - pharmacology | Myocardial Infarction - metabolism | Transcription Factors - genetics | Regeneration - physiology | Homeodomain Proteins - genetics | Transcription Factors - metabolism | Myocytes, Cardiac - pathology | Regeneration - drug effects | Animals | Myocytes, Cardiac - drug effects | NF-E2-Related Factor 2 - metabolism | Myocytes, Cardiac - metabolism | Heart Ventricles - metabolism | Mice | Wound Healing - physiology | Adaptor Proteins, Signal Transducing - metabolism | Heart Ventricles - drug effects | Heart | Physiological aspects | Genetic aspects | Regeneration (Biology) | Homeobox genes | Homeotic genes | Antioxidants | Transcription factors | Genetic regulation | Health aspects | Heart attack | Proteins | Heart attacks | Genes | DNA methylation | Cardiomyocytes | Kinases | Deoxyribonucleic acid--DNA
Journal Article
Circulation, ISSN 0009-7322, 06/2012, Volume 125, Issue 25, pp. 3170 - 3181
Journal Article
American Journal of Physiology - Heart and Circulatory Physiology, ISSN 0363-6135, 2015, Volume 309, Issue 9, pp. H1375 - H1389
Journal Article
Free Radical Biology and Medicine, ISSN 0891-5849, 12/2017, Volume 113, pp. 291 - 303
Myocardial injury and dysfunction are critical manifestations of sepsis. Previous studies have reported that liver X receptor (LXR) activation is protective... 
Heart | Oxidative stress | Liver X receptor | Endoplasmic-reticulum stress | Sepsis | Inflammation | SIRT1 | Apoptosis | BRAIN-INJURY | BIOCHEMISTRY & MOLECULAR BIOLOGY | RHO-KINASE | CARDIAC DYSFUNCTION | MESENCHYMAL STEM-CELLS | CECAL LIGATION | ENDOCRINOLOGY & METABOLISM | SEPTIC SHOCK | ORGAN DYSFUNCTION | NF-KAPPA-B | Heart Injuries - pathology | Tumor Necrosis Factor-alpha - metabolism | Transcription Factor CHOP - genetics | Heat Shock Transcription Factors - metabolism | Tumor Necrosis Factor-alpha - genetics | Hydrocarbons, Fluorinated - pharmacology | Male | Interleukin-1beta - genetics | Heart Injuries - drug therapy | Sirtuin 1 - genetics | HMGB1 Protein - genetics | Heat-Shock Proteins - genetics | Sepsis - drug therapy | Sepsis - pathology | Interleukin-1beta - metabolism | HMGB1 Protein - metabolism | Liver X Receptors - agonists | Myocardium - metabolism | Chemokine CCL2 - metabolism | Sirtuin 1 - deficiency | Interleukin-6 - metabolism | Forkhead Box Protein O1 - metabolism | Heart Injuries - genetics | Interleukin-6 - genetics | Signal Transduction | Heat-Shock Proteins - metabolism | Gene Expression Regulation | Heat Shock Transcription Factors - genetics | Chemokine CCL2 - genetics | Myocardium - pathology | Liver X Receptors - metabolism | Sulfonamides - pharmacology | Sepsis - genetics | Mice, Knockout | Sepsis - mortality | Animals | Survival Analysis | Peroxidase - genetics | Mice | Transcription Factor CHOP - metabolism | Forkhead Box Protein O1 - genetics | Heart Injuries - mortality | Anticholesteremic Agents - pharmacology | Liver X Receptors - genetics | Peroxidase - metabolism | Tumor proteins | Cardiology | Analysis | Mortality | Liver
Journal Article
Journal of the American Heart Association, ISSN 2047-9980, 03/2017, Volume 6, Issue 3, p. n/a
Background The cardiac microvascular system ischemia/reperfusion injury following percutaneous coronary intervention is a clinical thorny problem. This study... 
apoptosis | ischemia/reperfusion injury | endothelial cell | mitochondria | Endothelial cell | Mitochondria | Ischemia/reperfusion injury | Apoptosis | CARDIAC & CARDIOVASCULAR SYSTEMS | PERMEABILITY | HEXOKINASE | NO-REFLOW PHENOMENON | REPERFUSION | ISCHEMIA | ENDOTHELIAL-CELLS | ACUTE MYOCARDIAL-INFARCTION | CYTOCHROME-C RELEASE | CARDIOPROTECTION | Immunohistochemistry | Mitochondria, Heart - ultrastructure | Microvessels - physiopathology | Mitochondria, Heart - metabolism | Reactive Oxygen Species - metabolism | Mitochondrial Dynamics - genetics | Apoptosis - drug effects | Male | Mitochondrial Proteins - genetics | Chromatography, High Pressure Liquid | Microcirculation - drug effects | Voltage-Dependent Anion Channel 1 - biosynthesis | Mitochondrial Membrane Transport Proteins - biosynthesis | Mitochondrial Membrane Transport Proteins - genetics | DNA, Mitochondrial - genetics | Hexokinase - biosynthesis | Hexokinase - genetics | Mitochondria, Heart - genetics | Myocardial Reperfusion Injury - genetics | Cardiolipins - genetics | Disease Models, Animal | Oxidation-Reduction | Endothelial Cells - metabolism | Membrane Proteins - genetics | Cells, Cultured | Gene Expression Regulation | Mitochondrial Proteins - biosynthesis | Blotting, Western | Myocardial Reperfusion Injury - physiopathology | Myocardial Reperfusion Injury - metabolism | Membrane Proteins - biosynthesis | Animals | Mitochondrial Dynamics - drug effects | Myocytes, Cardiac - metabolism | Cardiolipins - biosynthesis | Mice | Myocytes, Cardiac - ultrastructure | Voltage-Dependent Anion Channel 1 - genetics | Endothelial Cells - drug effects
Journal Article
Science, ISSN 0036-8075, 12/2012, Volume 338, Issue 6114, pp. 1599 - 1603
The epicardium encapsulates the heart and functions as a source of multipotent progenitor cells and paracrine factors essential for cardiac development and... 
Heart | Transcription factors | HEK293 cells | Transgenic animals | RESEARCH ARTICLES | Neutrophils | Epicardium | Physical trauma | Gene expression | Embryos | Transgenic plants | CELLS | IMMUNITY | RETINOIC ACID | ZEBRAFISH | GRAINY-HEAD | MOUSE HEART | INTEGRITY | REGENERATION | MULTIDISCIPLINARY SCIENCES | BINDING PROTEIN | DROSOPHILA | Myocardial Infarction - genetics | WT1 Proteins - metabolism | Oligonucleotide Array Sequence Analysis | Heart - embryology | Male | Pericardium - metabolism | Neutrophil Infiltration | Ventricular Remodeling | Gene Expression Regulation, Developmental | Uroplakin III - genetics | Pericardium - embryology | Female | CCAAT-Enhancer-Binding Protein-delta - metabolism | CCAAT-Enhancer-Binding Proteins - genetics | Binding Sites | Myocardial Reperfusion Injury - genetics | WT1 Proteins - genetics | Organ Culture Techniques | CCAAT-Enhancer-Binding Proteins - metabolism | Heart - physiopathology | Myocardial Contraction | Signal Transduction | CCAAT-Enhancer-Binding Protein-beta - genetics | Gene Expression Regulation | Mice, Transgenic | Aldehyde Oxidoreductases - genetics | Myocardial Infarction - metabolism | CCAAT-Enhancer-Binding Protein-beta - metabolism | Pericardium - cytology | Aldehyde Oxidoreductases - metabolism | Myocardial Reperfusion Injury - metabolism | Animals | Enhancer Elements, Genetic | CCAAT-Enhancer-Binding Protein-delta - genetics | Mice | Models, Genetic | Uroplakin III - metabolism | Cellular signal transduction | Genetic aspects | Research | Genetic transcription | Regeneration (Biology) | Properties | Observations | Proteins | Signal transduction | Cardiovascular disease | Embryology | Rodents | Injury prevention | Activation | Mathematical models | Adults | Heart function | Protective | Injuries
Journal Article
Cardiovascular Research, ISSN 0008-6363, 09/2012, Volume 95, Issue 4, pp. 487 - 494
Innate mechanisms of inter-organ protection underlie the phenomenon of remote ischaemic preconditioning (RPc) in which episode(s) of ischaemia and reperfusion... 
Brain | Vagus nerve | Ischaemia/reperfusion injury | Preconditioning | Ischaemia | CARDIAC & CARDIOVASCULAR SYSTEMS | K-ATP CHANNELS | LIMB ISCHEMIA | MYOCARDIAL-ISCHEMIA | BRAIN-STEM | reperfusion injury | LENTIVIRAL VECTORS | CARDIOVASCULAR CONTROL | TRANSGENE EXPRESSION | RAT-HEART | AUTONOMIC NERVOUS-SYSTEM | Myocardial Infarction - genetics | Hindlimb | Receptors, G-Protein-Coupled - metabolism | Brain Stem - metabolism | Vagus Nerve - drug effects | Male | Receptors, Neuropeptide - metabolism | Drosophila Proteins - metabolism | Rhodopsin - metabolism | Recombinant Fusion Proteins - metabolism | Autonomic Fibers, Preganglionic - metabolism | Brain Stem - drug effects | Action Potentials | Myocardial Reperfusion Injury - pathology | Time Factors | Muscarinic Antagonists - pharmacology | Myocardial Infarction - pathology | Neuropeptides - pharmacology | Adenoviridae - genetics | Lentivirus - genetics | Myocardial Infarction - physiopathology | Neural Pathways - physiopathology | Myocardial Reperfusion Injury - genetics | Autonomic Fibers, Preganglionic - drug effects | Disease Models, Animal | Heart - innervation | Muscle, Skeletal - blood supply | Transduction, Genetic | Vagus Nerve - metabolism | Constriction | Rats | Receptors, Neuropeptide - genetics | Atropine - pharmacology | Myocardium - pathology | Myocardial Infarction - metabolism | Rats, Sprague-Dawley | Myocardial Reperfusion Injury - physiopathology | Vagus Nerve - physiopathology | Myocardial Reperfusion Injury - metabolism | Animals | Rhodopsin - genetics | Ischemic Preconditioning, Myocardial - methods | Brain Stem - physiopathology | Myocardial Infarction - prevention & control | Receptors, G-Protein-Coupled - genetics | Drosophila Proteins - genetics | Genetic Vectors | Myocardial Reperfusion Injury - prevention & control | Original
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 4/2009, Volume 106, Issue 15, pp. 6297 - 6302
Journal Article