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Free Radical Biology and Medicine, ISSN 0891-5849, 04/2011, Volume 50, Issue 7, pp. 777 - 793
The heart has complex mechanisms that facilitate the maintenance of an oxygen supply–demand balance necessary for its contractile function in response to... 
Heart failure | Reactive oxygen species | Mitochondria | Free radicals | NADPH oxidase | Cardiac myocyte | Redox signaling | Hypertrophy | HYPOXIA-INDUCIBLE FACTOR | NOX2-CONTAINING NADPH OXIDASE | NITRIC-OXIDE SYNTHASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | FACTOR-KAPPA-B | MITOCHONDRIAL PERMEABILITY TRANSITION | EMBRYONIC STEM-CELLS | RECEPTOR-STIMULATED HYPERTROPHY | ENDOCRINOLOGY & METABOLISM | INDUCED CARDIOMYOCYTE HYPERTROPHY | XANTHINE OXIDOREDUCTASE INHIBITION | RAT VENTRICULAR MYOCYTES | Excitation Contraction Coupling - physiology | Myocardial Ischemia - metabolism | Rabbits | Cell Proliferation | Reactive Oxygen Species - metabolism | Heart Diseases - metabolism | Oxidation-Reduction | Oxidative Stress | Heart Diseases - physiopathology | Humans | NADPH Oxidases - metabolism | Stress, Physiological | Rats | Mitochondria - metabolism | Hypertrophy - metabolism | Oxygen - metabolism | Hypertrophy - physiopathology | Animals | Myocytes, Cardiac - physiology | Myocardial Ischemia - physiopathology | Thioredoxins - metabolism | Mice | Cell Differentiation - physiology | ARC, apoptosis repressor with caspase recruitment domain | PKG, protein kinase G | AIF, apoptosis-inducing factor | Review | MAO-A, monoamine oxidase-A | MI, myocardial infarction | TNFα, tumor necrosis factor-α | ES, embryonic stem | GPCR, G-protein-coupled receptor | RyR, ryanodine receptor | PHD, prolyl hydroxylase dioxygenase | CTGF, connective tissue growth factor | mtDNA, mitochondrial DNA | ROS, reactive oxygen species | ETC, electron transport chain | HDAC, histone deacetylase | EB, embryoid body | Ca exchanger | G6PDH, glucose-6-phosphate dehydrogenase | PKC, protein kinase C | SR, sarcoplasmic reticulum | SERCA, sarcoplasmic reticulum calcium ATPase | VEGF, vascular endothelial growth factor | Hif, hypoxia-inducible factor | NOS, nitric oxide synthase | NCX, Na | MPTP, mitochondrial permeability transition pore | ECC, excitation–contraction coupling | CamKII, calmodulin kinase II | ER, endoplasmic reticulum | MMP, matrix metalloproteinase | PKA, protein kinase A | Trx1, thioredoxin1
Journal Article
Journal Article
Journal Article
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