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Nature, ISSN 0028-0836, 11/2012, Volume 491, Issue 7423, pp. 269 - 273
Myocardial cell death is initiated by excessive mitochondrial Ca2+ entry causing Ca2+ overload, mitochondrial permeability transition pore (mPTP) opening and... 
OXIDATION | HYPERTROPHY | APOPTOSIS | INNER MEMBRANE | II INHIBITION PROTECTS | MULTIDISCIPLINARY SCIENCES | CALCIUM UNIPORTER | IN-VIVO | CALMODULIN KINASE | FAILURE | KINASE-II | Mitochondria, Heart - metabolism | Apoptosis - drug effects | Calcium - metabolism | Cyclosporine - pharmacology | Mitochondria, Heart - pathology | Membrane Potential, Mitochondrial - drug effects | Heart Failure - prevention & control | Myocardium - metabolism | Membrane Potential, Mitochondrial - physiology | Female | Stress, Physiological - drug effects | Reperfusion Injury - metabolism | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism | Heart - physiopathology | Mitochondrial Membrane Transport Proteins - metabolism | Calcium - pharmacology | Reperfusion Injury - pathology | Reperfusion Injury - enzymology | Mice, Inbred C57BL | Mitochondria, Heart - enzymology | Mice, Transgenic | Myocardium - pathology | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - antagonists & inhibitors | Serine - metabolism | Heart Failure - drug therapy | Myocardium - enzymology | Animals | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - chemistry | Myocardial Infarction - drug therapy | Reperfusion Injury - prevention & control | Heart - drug effects | Mice | Myocardial Infarction - prevention & control | Heart failure | Cell death | Heart cells | Research | Mitochondrial myopathies | Properties | Observations | Protein kinases | Calmodulin | Proteins | Heart | Mitochondria | Heart attacks | Rodents | Homeostasis | Apoptosis
Journal Article
Human Pathology, ISSN 0046-8177, 2015, Volume 49, pp. 27 - 32
Summary Complex I deficiency causes Leigh syndrome, fatal infant lactic acidosis, and neonatal cardiomyopathy. Mutations in more than 100 nuclear DNA and... 
Pathology | Metabolic disease | Lethal neonatal lactic acidosis | Whole-exome sequencing | Mitochondriopathy | Complex I deficiency | ACAD9 defect | Mitochondrial hyperplasia | Multiorgan failure | DIAGNOSIS | CARDIOMYOPATHY | PATHOLOGY | GENE | DNA | EXPRESSION | Immunohistochemistry | Fibroblasts - enzymology | Diaphragm - pathology | Mitochondria, Heart - pathology | Electron Transport Complex I - deficiency | Humans | Hyperplasia | Male | Cardiomyopathy, Hypertrophic - enzymology | Acyl-CoA Dehydrogenases - genetics | Leigh Disease - pathology | Muscle Weakness - genetics | Amino Acid Metabolism, Inborn Errors - genetics | Autopsy | DNA Mutational Analysis | Electron Transport Complex I - genetics | Fatal Outcome | Muscle Weakness - pathology | Acyl-CoA Dehydrogenases - deficiency | Amino Acid Metabolism, Inborn Errors - pathology | Kidney Tubules - pathology | Infant, Newborn | Multiple Organ Failure - pathology | Acyl-CoA Dehydrogenase - genetics | Cardiomyopathy, Hypertrophic - genetics | Genetic Predisposition to Disease | Mitochondria, Liver - pathology | Mitochondria, Heart - enzymology | Fibroblasts - pathology | Leigh Disease - genetics | Acidosis, Lactic - pathology | Cardiomyopathy, Hypertrophic - diagnosis | Mitochondrial Diseases - enzymology | Phenotype | Acyl-CoA Dehydrogenase - deficiency | Kidney Tubules - enzymology | Acidosis - diagnosis | Multiple Organ Failure - enzymology | Acidosis - genetics | Amino Acid Metabolism, Inborn Errors - enzymology | Mitochondrial Diseases - pathology | Muscle Weakness - diagnosis | Acidosis, Lactic - genetics | Cause of Death | Acidosis, Lactic - enzymology | Amino Acid Metabolism, Inborn Errors - diagnosis | DNA, Mitochondrial - genetics | Muscle Weakness - enzymology | Transfection | Mitochondrial Diseases - genetics | Mitochondria, Muscle - enzymology | Mitochondria, Muscle - pathology | Leigh Disease - enzymology | Cells, Cultured | Multiple Organ Failure - genetics | Codon, Nonsense | Mitochondria, Liver - enzymology | Multiple Organ Failure - diagnosis | Diaphragm - enzymology | Acidosis - pathology | Leigh Disease - diagnosis | Acidosis - enzymology | Mitochondrial Diseases - diagnosis | Acidosis, Lactic - diagnosis | Cardiomyopathy, Hypertrophic - pathology | Infants (Newborn) | Muscles | Genetic aspects | Mitochondrial DNA | Liver | Heart | Urine | Cytochrome | Antigens | Enzymes | Cytomegalovirus | Cardiomyopathy | Data bases | Defects | Musculoskeletal system | Rodents | Fibroblasts | Oxidation | Mutation | Metabolic disorders | Deoxyribonucleic acid--DNA
Journal Article
Circulation research, ISSN 0009-7330, 2014, Volume 114, Issue 2, pp. 257 - 265
Journal Article
Circulation Research, ISSN 0009-7330, 04/2010, Volume 106, Issue 7, pp. 1253 - 1264
RATIONALE:NADPH oxidases are a major source of superoxide (O2) in the cardiovascular system. The function of Nox4, a member of the Nox family of NADPH... 
Aging | Oxidative stress | Reactive oxygen species | Superoxide | Apoptosis | Hypertrophy | CELLS | PRESSURE-OVERLOAD | CARDIAC & CARDIOVASCULAR SYSTEMS | hypertrophy | PHOSPHORYLATION | apoptosis | ANGIOTENSIN-II | FAMILY NADPH OXIDASES | FREE-RADICALS | NAD(P)H OXIDASE | reactive oxygen species | PERIPHERAL VASCULAR DISEASE | GENERATION | aging | superoxide | HEMATOLOGY | oxidative stress | Aconitate Hydratase - metabolism | Up-Regulation | Cysteine | Cell Proliferation | Uncoupling Agents - pharmacology | Oxidative Stress | Rats, Wistar | Ventricular Function, Left | Apoptosis - drug effects | Mitochondria, Heart - pathology | Humans | NADPH Oxidases - metabolism | Cardiomegaly - pathology | Mitochondria, Heart - drug effects | Myocytes, Cardiac - enzymology | Transfection | Ventricular Dysfunction, Left - genetics | Rotenone - pharmacology | Superoxides - metabolism | Ventricular Dysfunction, Left - pathology | NADPH Oxidases - genetics | Ventricular Dysfunction, Left - enzymology | Disease Models, Animal | Oxidation-Reduction | NADPH Oxidases - antagonists & inhibitors | Cells, Cultured | Enzyme Inhibitors - pharmacology | Mitochondria, Heart - enzymology | Cardiomegaly - physiopathology | Rats | Genotype | Mice, Transgenic | Cardiomegaly - enzymology | NADPH Oxidase 4 | Onium Compounds - pharmacology | NADH Dehydrogenase - metabolism | Ventricular Dysfunction, Left - physiopathology | Aging - pathology | Myocytes, Cardiac - pathology | Phenotype | Animals | Myocytes, Cardiac - drug effects | Fibrosis | Mice | Cardiomegaly - genetics | Aging - metabolism
Journal Article
Science, ISSN 0036-8075, 6/2005, Volume 308, Issue 5730, pp. 1909 - 1911
To determine the role of reactive oxygen species in mammalian longevity, we generated transgenic mice that overexpress human catalase localized to the... 
Antioxidants | Pathology | Mitochondria | Reactive oxygen species | Life span | Standardized tests | Transgenic animals | Reports | Mice | Longevity | Skeletal muscle | HEART | LONGEVITY | OXIDATIVE STRESS | CAENORHABDITIS-ELEGANS | DROSOPHILA-MELANOGASTER | THIOREDOXIN | INCREASE | MULTIDISCIPLINARY SCIENCES | SUPEROXIDE DISMUTASE/CATALASE MIMETICS | IN-VIVO | EXPRESSION | Aconitate Hydratase - metabolism | Mitochondria - enzymology | Superoxide Dismutase - genetics | Mitochondria, Heart - metabolism | Reactive Oxygen Species - metabolism | Myocardium - chemistry | Oxidative Stress | Humans | Cataract - pathology | Male | Deoxyguanosine - analysis | Cell Nucleus - enzymology | Cell Nucleus - metabolism | Muscle, Skeletal - chemistry | Aging | Female | Deoxyguanosine - analogs & derivatives | Superoxide Dismutase - metabolism | Free Radicals | Oxidation-Reduction | Signal Transduction | Catalase - genetics | Mitochondria, Heart - enzymology | Mice, Transgenic | Myocardium - pathology | Mitochondria - metabolism | Reverse Transcriptase Polymerase Chain Reaction | Hydrogen Peroxide - metabolism | Catalase - metabolism | DNA - chemistry | Animals | Peroxisomes - enzymology | Arteriosclerosis - pathology | Heart Diseases - pathology | Psychological aspects | Peroxisomes | Physiological aspects | Genetic aspects | Research | Properties | Health aspects | Molecules | Oxygen | Life expectancy | Rodents
Journal Article
Journal Article
Antioxidants & Redox Signaling, ISSN 1523-0864, 01/2013, Volume 18, Issue 1, pp. 5 - 18
Journal Article
Basic Research in Cardiology, ISSN 0300-8428, 5/2008, Volume 103, Issue 3, pp. 274 - 284
In the majority of studies, metformin has been demonstrated to cardioprotect diabetic patients, the mechanism of which is unclear. We hypothesized that... 
Medicine & Public Health | signal transduction | infarction | metformin | Cardiology | diabetes | reperfusion | Signal transduction | Infarction | Reperfusion | Diabetes | Metformin | COMPLEX I | RESPIRATORY-CHAIN | OXIDATIVE STRESS | CARDIAC & CARDIOVASCULAR SYSTEMS | MYOCARDIAL-INFARCTION | REPERFUSION INJURY | ACUTE CORONARY SYNDROMES | CELL-DEATH | DIABETES-MELLITUS | BYPASS SURGERY | CLINICAL-OUTCOMES | Diabetes Mellitus - enzymology | Diabetes Mellitus - pathology | Phosphorylation | Mitochondrial Membrane Transport Proteins - antagonists & inhibitors | Rats, Wistar | Ischemic Contracture - enzymology | Male | Phosphatidylinositol 3-Kinases - metabolism | Mitochondria, Heart - drug effects | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Myocardial Reperfusion Injury - enzymology | Dose-Response Relationship, Drug | Myocardial Reperfusion Injury - pathology | Hypoglycemic Agents - administration & dosage | Metformin - administration & dosage | Chromones - pharmacology | Proto-Oncogene Proteins c-akt - metabolism | Disease Models, Animal | Mitochondrial Membrane Transport Proteins - metabolism | Drug Administration Schedule | Metformin - pharmacology | Diabetes Mellitus - drug therapy | Mitochondria, Heart - enzymology | Morpholines - pharmacology | Myocardial Ischemia - prevention & control | Rats | Myocardium - pathology | Myocardial Ischemia - enzymology | Ischemic Contracture - prevention & control | Hypoglycemic Agents - pharmacology | Myocardial Ischemia - pathology | Myocardium - enzymology | Animals | Protein Kinase Inhibitors - pharmacology | Oxidative Stress - drug effects | Myocardial Reperfusion Injury - prevention & control | Ischemia
Journal Article