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Nature Medicine, ISSN 1078-8956, 02/2016, Volume 22, Issue 2, pp. 175 - 182
Regulated necrosis (necroptosis) and apoptosis are crucially involved in severe cardiac pathological conditions, including myocardial infarction,... 
MEDICINE, RESEARCH & EXPERIMENTAL | ISCHEMIA/REPERFUSION INJURY | BIOCHEMISTRY & MOLECULAR BIOLOGY | REPERFUSION INJURY | HEART-FAILURE | RECEPTOR INTERACTING PROTEIN-3 | MIXED LINEAGE KINASE | PROGRAMMED NECROSIS | DOMAIN-LIKE | CELL-DEATH | CELL BIOLOGY | MITOCHONDRIAL PERMEABILITY TRANSITION | INDEPENDENT ACTIVATION | Immunohistochemistry | Myocardial Ischemia - genetics | Receptor-Interacting Protein Serine-Threonine Kinases - metabolism | Phosphorylation | Antibiotics, Antineoplastic - toxicity | Reactive Oxygen Species | Oxidative Stress | Apoptosis - genetics | Necrosis - pathology | Membrane Potential, Mitochondrial | Myocardial Reperfusion Injury - genetics | Real-Time Polymerase Chain Reaction | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism | In Situ Nick-End Labeling | Mitochondrial Membrane Transport Proteins - metabolism | Cell Survival | Mice, Inbred C57BL | Rats | Heart Failure - genetics | Heart Failure - pathology | Rats, Sprague-Dawley | Blotting, Western | Doxorubicin - toxicity | Mice, Knockout | Myocardial Ischemia - pathology | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - genetics | Microscopy, Confocal | Myocardial Reperfusion Injury - metabolism | Myocytes, Cardiac - pathology | Receptor-Interacting Protein Serine-Threonine Kinases - genetics | Animals | Myocardial Ischemia - complications | Necrosis - etiology | Myocytes, Cardiac - metabolism | Mice | Necrosis - genetics | Heart Failure - chemically induced | Oxidative stress | Medical research | Physiological aspects | Medicine, Experimental | Research | Heart diseases | Necrosis | Apoptosis | Signal transduction | Cardiovascular disease | Cardiomyocytes | Ischemia | Index Medicus
Journal Article
Journal Article
JACC (Journal of the American College of Cardiology), ISSN 0735-1097, 2013, Volume 61, Issue 4, pp. 427 - 436
Objectives The aim of this study was to test the hypothesis that elevated nonfasting remnant cholesterol is a causal risk factor for ischemic heart disease... 
Cardiovascular | Internal Medicine | atherosclerosis | cardiovascular disease | lipoproteins | myocardial infarction | CARDIAC & CARDIOVASCULAR SYSTEMS | MYOCARDIAL-INFARCTION | PREDICTIVE-VALUE | MENDELIAN RANDOMIZATION | PARTICLE CHOLESTEROL | DIABETES-MELLITUS | DENSITY-LIPOPROTEIN CHOLESTEROL | NONFASTING TRIGLYCERIDES | CARDIOVASCULAR-DISEASE | HDL CHOLESTEROL | CORONARY-ARTERY-DISEASE | Myocardial Ischemia - genetics | Myocardial Ischemia - metabolism | Lipoproteins, HDL - genetics | Humans | Middle Aged | Risk Factors | Lipoproteins, HDL - metabolism | Genotype | Male | Data Collection | Cholesterol - metabolism | Cholesterol - genetics | Genetic Variation - physiology | Triglycerides - metabolism | Time Factors | Denmark - epidemiology | Female | Aged | Triglycerides - genetics | Causality | Odds Ratio | Myocardial Ischemia - epidemiology | Analysis and chemistry | Blood cholesterol | Low density lipoproteins | Atherosclerosis | Myocardial ischemia | Universities and colleges | Heart attack | Risk factors | Blood | Cholesterol | Heart | Lipoproteins (low density) | Cardiovascular disease | Density | Confidence intervals | Variables | Randomization | Ischemia | Population | Blood pressure | Heart diseases | Lipoproteins (high density) | Age | Deoxyribonucleic acid--DNA | Hypertension | Enzymes | Health risks | Triglycerides | Risk analysis | Apolipoproteins | Low density lipoprotein | Coronary artery disease | Studies | Genetic variance | Lipoproteins | Diabetes | Cardiovascular diseases | Index Medicus | Abridged Index Medicus
Journal Article
Journal of Molecular and Cellular Cardiology, ISSN 0022-2828, 2011, Volume 52, Issue 1, pp. 175 - 184
Journal Article
Circulation, ISSN 0009-7322, 07/2010, Volume 122, Issue 1, pp. 11 - 19
Background-Hydrogen sulfide (H2S) is an endogenous signaling molecule with potent cytoprotective effects. The present study evaluated the therapeutic potential... 
heart failure | OXIDATIVE STRESS | CARDIAC & CARDIOVASCULAR SYSTEMS | cystathionine gamma-Lyase | myocardial infarction | REPERFUSION INJURY | MYOCARDIAL ISCHEMIA/REPERFUSION INJURY | ischemia | PROTECTS | INFARCTION | REACTIVE OXYGEN | hydrogen sulfide | PHASE-2 ENZYMES | ENDOTHELIAL-CELLS | PERIPHERAL VASCULAR DISEASE | CARDIOPROTECTION | HEMATOLOGY | EXPRESSION | Myocardial Ischemia - genetics | Body Weight | Ventricular Function, Left - genetics | Male | Vasodilation - genetics | Ventricular Dysfunction, Left - genetics | Nuclear Respiratory Factor 1 - metabolism | Cystathionine gamma-Lyase - genetics | Heart Failure - etiology | Mice, Inbred C57BL | NF-E2-Related Factor 2 - drug effects | Organ Size | Heart Failure - genetics | Mice, Transgenic | Survival Rate | Sulfates - pharmacology | Cardiomegaly - enzymology | Nuclear Respiratory Factor 1 - drug effects | Heart Failure - drug therapy | Gene Expression Regulation, Enzymologic | Hydrogen Sulfide - therapeutic use | Animals | Cardiomegaly - prevention & control | Myocardial Ischemia - complications | NF-E2-Related Factor 2 - metabolism | Mice | Vasodilation - drug effects | Heart failure | Hydrogen sulfide | Animal experimentation | Care and treatment | Usage | Myocardial ischemia | Genetic aspects | Health aspects | Index Medicus | Abridged Index Medicus | cystathionine γ-Lyase
Journal Article
Circulation Research, ISSN 0009-7330, 05/2012, Volume 110, Issue 11, pp. 1465 - 1473
Journal Article
Apoptosis, ISSN 1360-8185, 7/2016, Volume 21, Issue 7, pp. 809 - 824
Recently, we demonstrated that melatonin reduced protein kinase RNA (PKR)-like ER kinase (PERK)-eukaryotic initiation factor 2 alpha (eIF2α)-activating... 
Biochemistry, general | Melatonin | Biomedicine | Myocardial ischemia–reperfusion injury | Survivor activating factor enhancement pathway | Cancer Research | Oncology | Reperfusion injury salvage kinase pathway | Cell Biology | Virology | Endoplasmic reticulum stress | H9C2 CARDIOMYOBLAST CELLS | ISCHEMIA/REPERFUSION INJURY | INDUCED APOPTOSIS | BIOCHEMISTRY & MOLECULAR BIOLOGY | Myocardial ischemia-reperfusion injury | CARDIAC DYSFUNCTION | DIABETIC-RATS | CELLULAR STRESS | CELL BIOLOGY | IN-VITRO | SIGNALING PATHWAY | CARDIOVASCULAR-DISEASES | ACTIVATES STAT3 | Myocardial Ischemia - genetics | Myocardial Ischemia - metabolism | Phosphorylation | Oxidative Stress | eIF-2 Kinase - metabolism | Humans | Male | Phosphatidylinositol 3-Kinases - metabolism | Melatonin - administration & dosage | Myocardial Reperfusion Injury - enzymology | Myocardium - metabolism | Eukaryotic Initiation Factor-2 - metabolism | Myocardial Reperfusion Injury - drug therapy | Myocardial Reperfusion Injury - genetics | eIF-2 Kinase - genetics | Signal Transduction | Mice, Inbred C57BL | Activating Transcription Factor 4 - genetics | Glycogen Synthase Kinase 3 - metabolism | Phosphatidylinositol 3-Kinases - genetics | Myocardial Reperfusion Injury - metabolism | Animals | Activating Transcription Factor 4 - metabolism | Glycogen Synthase Kinase 3 - genetics | Endoplasmic Reticulum Stress | Eukaryotic Initiation Factor-2 - genetics | Myocardial Ischemia - surgery | Index Medicus
Journal Article
PLoS ONE, ISSN 1932-6203, 10/2013, Volume 8, Issue 10, pp. e75872 - e75872
Background: Ischemic postconditioning (IPost) protects the reperfused heart from infarction which has drawn much attention recently. However, studies to date... 
HEART | PERCUTANEOUS CORONARY INTERVENTION | ACTIVATION | CARDIOMYOCYTE APOPTOSIS | NITRIC-OXIDE SYNTHASE | MULTIDISCIPLINARY SCIENCES | ATTENUATION | ACUTE MYOCARDIAL-INFARCTION | CARDIOPROTECTION | EXPRESSION | MICRORNA | Myocardial Ischemia - genetics | Oligonucleotides - genetics | Apoptosis - drug effects | Gene Expression Regulation - genetics | Enzyme Inhibitors - pharmacology | PTEN Phosphohydrolase - metabolism | Apoptosis - genetics | Male | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Myocardial Ischemia - pathology | Gene Expression Regulation - drug effects | Myocytes, Cardiac - pathology | Animals | Myocytes, Cardiac - drug effects | Reperfusion Injury - prevention & control | Signal Transduction - drug effects | Ventricular Dysfunction, Left - genetics | Myocardial Ischemia - therapy | Ventricular Dysfunction, Left - pathology | Ischemic Postconditioning | Myocardial Ischemia - physiopathology | Mice | MicroRNAs - genetics | Proto-Oncogene Proteins c-akt - metabolism | Heart | Ischemia | MicroRNA | Myocardial infarction | Heart attacks | Myocardial ischemia | AKT protein | Kinases | Signal transduction | Reperfusion | Rodents | Cardiology | Heart diseases | Cytokines | MiRNA | Cardiomyocytes | Gene expression | Molecular chains | 1-Phosphatidylinositol 3-kinase | Signaling | Ostomy | Injury prevention | Hospitals | Molecular modelling | MicroRNAs | Infarction | Ventricle | Laboratory animals | PTEN protein | Apoptosis | Index Medicus
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 02/2016, Volume 291, Issue 6, pp. 2566 - 2575
Journal Article