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Nature (London), ISSN 1476-4687, 2013, Volume 502, Issue 7471, pp. 372 - 376
Ca2+/calmodulin-dependent protein kinase II (CaMKII) is an enzyme with important regulatory functions in the heart and brain, and its chronic activation can be... 
N-ACETYLGLUCOSAMINE | MYOCYTES | MULTIDISCIPLINARY SCIENCES | HEART-FAILURE | CARDIAC-HYPERTROPHY | RECEPTOR | CYTOSOLIC PROTEINS | CARDIOMYOCYTES | MELLITUS | CA2+/CALMODULIN-DEPENDENT PROTEIN-KINASE | INSIGHT | Calcium - metabolism | Humans | Brain - enzymology | Hyperglycemia - complications | Glycosylation - drug effects | Acetylglucosamine - metabolism | Myocytes, Cardiac - enzymology | Diazooxonorleucine - pharmacology | Sarcoplasmic Reticulum - metabolism | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism | Arrhythmias, Cardiac - metabolism | Diabetes Complications - metabolism | Rats | Glucose - pharmacology | Enzyme Activation - drug effects | Sulfonamides - pharmacology | Myocardium - cytology | Brain - drug effects | Hyperglycemia - metabolism | Myocardium - enzymology | Animals | Arrhythmias, Cardiac - enzymology | Glucose - metabolism | Hyperglycemia - enzymology | Myocytes, Cardiac - metabolism | Arrhythmias, Cardiac - complications | Diabetes Complications - enzymology | Mice | Benzylamines - pharmacology | Enzymes | Medical research | Arrhythmia | Protein biosynthesis | Glycosylation | Research | Risk factors | Complications and side effects | Hyperglycemia | Physiological aspects | Medicine, Experimental | Regulation | Protein kinases | Proteins | Brain | Phosphorylation | Rodents | Cardiomyocytes | Diabetes | Kinases
Journal Article
Nature communications, ISSN 2041-1723, 2015, Volume 6, Issue 1, p. 6656
.... Here we show that HKL blocks agonist-induced and pressure overload-mediated, cardiac hypertrophic responses, and ameliorates pre-existing cardiac hypertrophy, in mice... 
METABOLISM | GENE | SIRT3-MEDIATED DEACETYLATION | PATHWAY | PROTEIN-KINASE | MULTIDISCIPLINARY SCIENCES | HOMOLOG | AKT | SIRTUINS | CALORIE RESTRICTION | CELL-DEATH | Mitochondria - enzymology | Fibroblasts - enzymology | Superoxide Dismutase - genetics | Reactive Oxygen Species - metabolism | Sirtuin 3 - metabolism | Myofibroblasts - enzymology | Superoxide Dismutase - antagonists & inhibitors | Cardiomegaly - pathology | Isoproterenol | Lignans - pharmacology | Myocytes, Cardiac - enzymology | Phenylephrine - pharmacology | Biphenyl Compounds - pharmacology | Membrane Proteins - metabolism | Superoxide Dismutase - metabolism | Myofibroblasts - pathology | Sirtuin 3 - genetics | Signal Transduction | Membrane Proteins - genetics | Carrier Proteins - antagonists & inhibitors | Gene Expression Regulation | Adenosine Triphosphatases - metabolism | Myocardium - pathology | Cardiotonic Agents - pharmacology | Mitochondria - drug effects | Mitochondria - pathology | Fibroblasts - pathology | Myofibroblasts - drug effects | Adenosine Triphosphatases - antagonists & inhibitors | Carrier Proteins - genetics | Myocytes, Cardiac - pathology | Acetylation - drug effects | Myocardium - enzymology | Reactive Oxygen Species - antagonists & inhibitors | Animals | Cardiomegaly - prevention & control | Carrier Proteins - metabolism | Myocytes, Cardiac - drug effects | Membrane Proteins - antagonists & inhibitors | Cell Differentiation - drug effects | Fibroblasts - drug effects | Cardiomegaly - chemically induced | Adenosine Triphosphatases - genetics | Cell Proliferation - drug effects | Mice | Enzyme Activation | Primary Cell Culture | Cardiomegaly - genetics
Journal Article
Circulation research, ISSN 1524-4571, 2013, Volume 112, Issue 4, pp. 675 - 688
RATIONALE:Matrix metalloproteinase (MMP)-28 regulates the inflammatory and extracellular matrix responses in cardiac aging, but the roles of MMP-28 after myocardial infarction (MI... 
fibroblast | MMP-28 | inflammation | macrophage phenotype | myocardial infarction | LYSYL OXIDASE | CARDIAC & CARDIOVASCULAR SYSTEMS | TGF-BETA | VENTRICULAR-FUNCTION | HEART-FAILURE | CORONARY MICROEMBOLIZATION | REPAIR | MATRIX-METALLOPROTEINASE-9 | PERIPHERAL VASCULAR DISEASE | EPILYSIN MMP-28 | TNF-ALPHA | TARGETED DELETION | HEMATOLOGY | Myocardial Infarction - blood | Cell Adhesion Molecules - genetics | Cicatrix - etiology | Extracellular Matrix Proteins - biosynthesis | Male | Matrix Metalloproteinases, Secreted - deficiency | Pulmonary Edema - etiology | Myocytes, Cardiac - enzymology | Myofibroblasts - metabolism | Ventricular Dysfunction, Left - enzymology | Ventricular Remodeling - genetics | Female | Myocardial Infarction - physiopathology | Transcription, Genetic | Cytokines - genetics | Heart Rupture - enzymology | Receptors, Cytokine - genetics | Matrix Metalloproteinase 9 - blood | Myocardial Infarction - enzymology | Macrophage Activation - physiology | Macrophages - classification | Cell Adhesion Molecules - biosynthesis | Receptors, Cytokine - biosynthesis | Extracellular Matrix Proteins - genetics | Mice, Inbred C57BL | Gene Expression Regulation | Ventricular Dysfunction, Left - etiology | Inflammation | Ventricular Remodeling - physiology | Macrophages - enzymology | Mice, Knockout | Collagen - metabolism | Myocardial Infarction - complications | Heart Rupture - etiology | Animals | Pulmonary Edema - enzymology | Matrix Metalloproteinases, Secreted - genetics | Matrix Metalloproteinases, Secreted - physiology | Protein-Lysine 6-Oxidase - metabolism | Cicatrix - enzymology | Mice | Cytokines - biosynthesis
Journal Article
Journal of the American College of Cardiology, ISSN 0735-1097, 2016, Volume 68, Issue 22, pp. 2454 - 2464
Journal Article
Circulation research, ISSN 0009-7330, 04/2010, Volume 106, Issue 7, pp. 1253 - 1264
.... Neither transgenic mice with cardiac specific overexpression of Nox4 (Tg-Nox4) nor those with catalytically inactive Nox4 (Tg-Nox4-P437H... 
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
Journal Article
Circulation research, ISSN 1524-4571, 2013, Volume 113, Issue 8, pp. 1004 - 1012
RATIONALE:Efficient clearance of apoptotic cells (efferocytosis) is a prerequisite for inflammation resolution and tissue repair. After myocardial infarction,... 
Myocardial infarction | Efferocytosis | Inflammation | Macrophages | Phagocytosis | phagocytosis | CLEARANCE | CELL ACCUMULATION | CARDIAC & CARDIOVASCULAR SYSTEMS | PHOSPHATIDYLSERINE RECEPTOR | efferocytosis | myocardial infarction | HEART-FAILURE | PLAQUE NECROSIS | ACCELERATES ATHEROSCLEROSIS | MEDIATED PHAGOCYTOSIS | MICE LACKING | macrophages | inflammation | ACUTE MYOCARDIAL-INFARCTION | PERIPHERAL VASCULAR DISEASE | MER | HEMATOLOGY | Inflammation - pathology | Myocardial Infarction - genetics | CD36 Antigens - deficiency | CD36 Antigens - genetics | Ventricular Function, Left | Myocytes, Cardiac - immunology | Coculture Techniques | Male | Wound Healing | Myocardial Infarction - immunology | Recovery of Function | Myocytes, Cardiac - enzymology | Ventricular Remodeling | Time Factors | Myocardial Infarction - pathology | c-Mer Tyrosine Kinase | Bone Marrow Transplantation | Antigens, Ly - metabolism | Female | Myocardial Infarction - physiopathology | Macrophages - immunology | Disease Models, Animal | Myocardial Infarction - enzymology | Myocardial Contraction | Proto-Oncogene Proteins - metabolism | Receptor Protein-Tyrosine Kinases - deficiency | Macrophages - pathology | Signal Transduction | Mice, Inbred C57BL | Cells, Cultured | Proto-Oncogene Proteins - genetics | Inflammation - immunology | Proto-Oncogene Proteins - deficiency | Receptor Protein-Tyrosine Kinases - metabolism | Transplantation Chimera | Macrophages - enzymology | Mice, Knockout | Myocytes, Cardiac - pathology | Animals | Receptor Protein-Tyrosine Kinases - genetics | Inflammation - genetics | Mice | Inflammation - enzymology | Apoptosis
Journal Article
The Journal of cell biology, ISSN 1540-8140, 2009, Volume 186, Issue 6, pp. 805 - 816
The dynamin-related guanosine triphosphatase Drp1 mediates the division of mitochondria and peroxisomes. To understand the in vivo function of Drp1, complete... 
Cerebellum | Mitochondria | Peroxisomes | Neurons | Antibodies | Cytochromes | Reports | Mice | Giant cells | Embryos | Apoptosis | OUTER-MEMBRANE | APOPTOSIS | DOMINANT OPTIC ATROPHY | FUSION | MITOCHONDRIAL FISSION MACHINERY | SYNAPSE FORMATION | CYTOCHROME-C RELEASE | PROTEIN DLP1 | DIVISION | CELL-DEATH | CELL BIOLOGY | Mitochondria - enzymology | Trophoblasts - ultrastructure | Fibroblasts - enzymology | Giant Cells - enzymology | Microtubule-Associated Proteins - genetics | Microtubule-Associated Proteins - metabolism | Trophoblasts - enzymology | Cerebellum - enzymology | Fibroblasts - ultrastructure | Mitochondria - ultrastructure | Purkinje Cells - enzymology | Cerebellum - embryology | Myocytes, Cardiac - enzymology | Adenosine Triphosphate - metabolism | Ultrasonography | Microtubule-Associated Proteins - deficiency | Purkinje Cells - diagnostic imaging | Mice, Inbred C57BL | Cells, Cultured | Dynamins | Gestational Age | Mice, Knockout | Organogenesis | Animals | GTP Phosphohydrolases - metabolism | GTP Phosphohydrolases - genetics | GTP Phosphohydrolases - deficiency | Peroxisomes - enzymology | Cerebellum - ultrastructure | Mitochondrial Size | Myocytes, Cardiac - ultrastructure | Organelle Shape | Peroxisomes - ultrastructure | Giant Cells - ultrastructure | Physiological aspects | Brain | Embryonic development | Research | Guanosine triphosphatase
Journal Article
Antioxidants & redox signaling, ISSN 1523-0864, 03/2013, Volume 18, Issue 9, pp. 124 - 1041
Significance: Oxidative stress is involved in the pathogenesis of heart failure but clinical antioxidant trials have been unsuccessful. This may be because... 
Forum Review Articles | OXIDE SYNTHASE ACTIVATION | RESPIRATORY BURST OXIDASE | INDUCED CARDIAC DYSFUNCTION | CHRONIC GRANULOMATOUS-DISEASE | DEHYDROGENASE-DERIVED NADPH | BIOCHEMISTRY & MOLECULAR BIOLOGY | ENDOCRINOLOGY & METABOLISM | NUCLEOTIDE EXCHANGE FACTOR | INDUCED CARDIOMYOCYTE HYPERTROPHY | VASCULAR SMOOTH-MUSCLE | SIGNAL-REGULATING KINASE-1 | EXPERIMENTAL MYOCARDIAL-INFARCTION | Fibroblasts - enzymology | Hypertrophy, Left Ventricular - enzymology | Reactive Oxygen Species | Oxidative Stress | Heart Failure - enzymology | Humans | Molecular Targeted Therapy | Leukocytes - enzymology | Neovascularization, Pathologic - etiology | Myocytes, Cardiac - enzymology | NADPH Oxidases - deficiency | Membrane Glycoproteins - physiology | NADPH Oxidases - genetics | Models, Cardiovascular | Hypertrophy, Left Ventricular - etiology | NADPH Oxidases - antagonists & inhibitors | Aldosterone - physiology | Arrhythmias, Cardiac - etiology | Heart Failure - pathology | NADPH Oxidase 2 | Heart Failure - drug therapy | Hydrogen Peroxide - metabolism | Animals | Protein Isoforms | Fibrosis | Arrhythmias, Cardiac - enzymology | Mice | Enzyme Activation | NADPH Oxidases - physiology | Subcellular Fractions - enzymology | Angiotensin II - physiology | Membrane Glycoproteins - deficiency | Apoptosis | Oxidases | Heart failure | Physiological aspects | Development and progression | NADP (Coenzyme) | Forum Review
Journal Article