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Circulation, ISSN 0009-7322, 2012, Volume 126, Issue 7, pp. 830 - 839
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 | Index Medicus
Journal Article
Journal Article
Circulation, ISSN 0009-7322, 05/2009, Volume 119, Issue 19, pp. 2568 - 2577
Background-Some studies have shown that metformin activates AMP-activated protein kinase (AMPK) and has a potent cardioprotective effect against... 
Heart failure | Metformin | AMP-activated protein kinase | Nitric oxide | heart failure | nitric oxide | CARDIAC & CARDIOVASCULAR SYSTEMS | ENDOTHELIAL NO SYNTHASE | BLOOD-GLUCOSE | metformin | ENDOPLASMIC-RETICULUM STRESS | DILATED CARDIOMYOPATHY | CONSCIOUS DOGS | NITRIC-OXIDE PRODUCTION | MYOCARDIAL FATTY-ACID | IN-VIVO | PERIPHERAL VASCULAR DISEASE | INDUCED CARDIAC-HYPERTROPHY | GLUCOSE-UPTAKE | HEMATOLOGY | Metformin - therapeutic use | Rats, Wistar | Apoptosis - drug effects | Heart Failure - enzymology | Nitric Oxide Synthase Type III - biosynthesis | Natriuretic Peptides - biosynthesis | Aminoimidazole Carboxamide - pharmacology | Cardiotonic Agents - therapeutic use | Myocytes, Cardiac - enzymology | Ribonucleotides - pharmacology | Protein Processing, Post-Translational - drug effects | Ventricular Dysfunction, Left - genetics | Ultrasonography | Ventricular Dysfunction, Left - enzymology | Heart Failure - diagnostic imaging | Phosphorylation - drug effects | Drug Evaluation, Preclinical | Transforming Growth Factor beta1 - biosynthesis | Natriuretic Peptides - genetics | Pyrazoles - pharmacology | Nitric Oxide - biosynthesis | Cells, Cultured - drug effects | AMP-Activated Protein Kinases - antagonists & inhibitors | Insulin Resistance | Rats | Transforming Growth Factor beta1 - genetics | Pyrimidines - pharmacology | Nitric Oxide Synthase Type III - genetics | Cells, Cultured - enzymology | Disease Progression | Ventricular Dysfunction, Left - diagnostic imaging | Heart Failure - drug therapy | Gene Expression Regulation - drug effects | AMP-Activated Protein Kinases - physiology | Animals | Myocytes, Cardiac - drug effects | Ventricular Dysfunction, Left - drug therapy | Aminoimidazole Carboxamide - analogs & derivatives | Dogs | Fibrosis | Oxidative Stress - drug effects | Prevention | Oxidative stress | Usage | Demographic aspects | Animal models in research | Physiological aspects | Dosage and administration | Cyclic adenylic acid | Research | Protein kinases | Index Medicus | Abridged Index Medicus
Journal Article
Circulation Research, ISSN 0009-7330, 01/2010, Volume 106, Issue 1, pp. 193 - 202
Journal Article
Circulation, ISSN 0009-7322, 03/2013, Volume 127, Issue 10, pp. 1116 - 1127
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 6/2011, Volume 108, Issue 23, pp. 9572 - 9577
Journal Article
Circulation, ISSN 0009-7322, 01/2009, Volume 119, Issue 3, pp. 408 - 416
Journal Article
Journal Article
Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 04/2010, Volume 30, Issue 4, pp. 724 - 732
Journal Article
Circulation research, ISSN 0009-7330, 2014, Volume 114, Issue 2, pp. 257 - 265
Journal Article
Cell, ISSN 0092-8674, 2005, Volume 123, Issue 1, pp. 25 - 35
Phosphodiesterases (PDEs) regulate the local concentration of 3′,5′ cyclic adenosine monophosphate (cAMP) within cells. cAMP activates the cAMP-dependent... 
PROTEIN-KINASE-A | CYCLIC-AMP | CAMP-SPECIFIC PHOSPHODIESTERASE | SUDDEN-DEATH | PHOSPHORYLATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | CARDIAC MYOCYTES | VENTRICULAR MYOCYTES | RELEASE | FAILING HEARTS | CA2+ LEAK | CELL BIOLOGY | Phosphorylation | Arrhythmias, Cardiac - chemically induced | Cyclic Nucleotide Phosphodiesterases, Type 4 | Heart Failure - enzymology | Cyclic Nucleotide Phosphodiesterases, Type 3 | Ryanodine Receptor Calcium Release Channel - metabolism | Myocytes, Cardiac - enzymology | 3',5'-Cyclic-AMP Phosphodiesterases - deficiency | Arrhythmias, Cardiac - genetics | Disease Models, Animal | Cyclic AMP-Dependent Protein Kinases - metabolism | Enzyme Inhibitors - adverse effects | 3',5'-Cyclic-AMP Phosphodiesterases - metabolism | Heart Failure - genetics | Mice, Transgenic | 3',5'-Cyclic-AMP Phosphodiesterases - genetics | Mice, Knockout | Myocardium - enzymology | Animals | 3',5'-Cyclic-AMP Phosphodiesterases - antagonists & inhibitors | Muscle Contraction - physiology | Arrhythmias, Cardiac - enzymology | Mice | Heart Failure - chemically induced | Macromolecular Substances - metabolism | Heart failure | Cyclic adenylic acid | Research | Arrhythmia | Phosphodiesterases | Risk factors | Medical colleges | Medical societies | Cardiac patients | Esterases | Adenylic acid | Protein kinases | Heart attack | Index Medicus
Journal Article