Superoxide production by NAD(P)H oxidase and mitochondria is increased in genetically obese and hyperglycemic rat heart and aorta before the development of cardiac dysfunction. The role of glucose-6-phosphate dehydrogenase-derived NADPH.

Superoxide production by NAD(P)H oxidase and mitochondria is increased in genetically obese and hyperglycemic rat heart and aorta before the development of cardiac dysfunction. The role of glucose-6-phosphate dehydrogenase-derived NADPH.

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http://www.wikidata.org/entity/Q37264479

Q37264479

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Obesity, metabolic dysfunction, and cardiac fibrosis: pathophysiological pathways, molecular mechanisms, and therapeutic opportunities Diabetic cardiomyopathy: bench to bedside NADPH oxidases in heart failure: poachers or gamekeepers?Interplay of oxidative, nitrosative/nitrative stress, inflammation, cell death and autophagy in diabetic cardiomyopathy Cardiac dysfunction and oxidative stress in the metabolic syndrome: an update on antioxidant therapies Targeting the redox balance in inflammatory skin conditions Glucose-6-phosphate dehydrogenase and NADPH redox regulates cardiac myocyte L-type calcium channel activity and myocardial contractile function Diabetic cardiomyopathy: pathophysiology and clinical features Obesity and insulin resistance induce early development of diastolic dysfunction in young female mice fed a Western diet.Role of NAD(P)H oxidase in superoxide generation and endothelial dysfunction in Goto-Kakizaki (GK) rats as a model of nonobese NIDDM.Analysis of oxidative stress enzymes and structural and functional proteins on human aortic tissue from different aortopathies.Diabetic cardiomyopathy, causes and effects.Targeting the Pentose Phosphate Pathway in Syndrome X-related Cardiovascular Complications.Impact of glucose-6-phosphate dehydrogenase deficiency on the pathophysiology of cardiovascular disease.Hyperthermia-induced Hsp90·eNOS preserves mitochondrial respiration in hyperglycemic endothelial cells by down-regulating Glut-1 and up-regulating G6PD activity.Involvement of signaling molecules on na/h exchanger-1 activity in human monocytes.Rodent models for metabolic syndrome research.Chronically elevated glucose compromises myocardial mitochondrial DNA integrity by alteration of mitochondrial topoisomerase function.Vascular Nitric Oxide: Formation and Function.Overnutrition and the Cardiorenal Syndrome: Use of a Rodent Model to Examine Mechanisms.Pulmonary arterial dysfunction in insulin resistant obese Zucker rats.MicroRNA-1 aggravates cardiac oxidative stress by post-transcriptional modification of the antioxidant network Metabolic alterations induce oxidative stress in diabetic and failing hearts: different pathways, same outcome.Adaptive mechanisms to compensate for overnutrition-induced cardiovascular abnormalities.Glucose-6-phosphate dehydrogenase, NADPH, and cell survival.High-sugar intake does not exacerbate metabolic abnormalities or cardiac dysfunction in genetic cardiomyopathy Prolonged diet induced obesity has minimal effects towards brain pathology in mouse model of cerebral amyloid angiopathy: implications for studying obesity-brain interactions in mice.Inflammatory cytokines as predictive markers for early detection and progression of diabetic nephropathy Effects of glucose-6-phosphate dehydrogenase deficiency on the metabolic and cardiac responses to obesogenic or high-fructose diets.Arterial Smooth Muscle Mitochondria Amplify Hydrogen Peroxide Microdomains Functionally Coupled to L-Type Calcium Channels.Glucose-6-Phosphate Dehydrogenase Enhances Antiviral Response through Downregulation of NADPH Sensor HSCARG and Upregulation of NF-κB Signaling Diabetes-associated cardiac fibrosis: Cellular effectors, molecular mechanisms and therapeutic opportunities.Alterations in glutathione redox metabolism, oxidative stress, and mitochondrial function in the left ventricle of elderly Zucker diabetic fatty rat heart.Type II diabetes increases mitochondrial DNA mutations in the left ventricle of the Goto-Kakizaki diabetic rat.Metabolic dysfunction in diabetic cardiomyopathy.Inflammation, glucose, and vascular cell damage: the role of the pentose phosphate pathway.Rotenone-stimulated superoxide release from mitochondrial complex I acutely augments L-type Ca2+ current in A7r5 aortic smooth muscle cells.Coronary endothelial dysfunction and mitochondrial reactive oxygen species in type 2 diabetic mice.Mechanisms of endothelial dysfunction in obesity-associated hypertension.A high-fat diet increases adiposity but maintains mitochondrial oxidative enzymes without affecting development of heart failure with pressure overload.

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Superoxide production by NAD(P)H oxidase and mitochondria is increased in genetically obese and hyperglycemic rat heart and aorta before the development of cardiac dysfunction. The role of glucose-6-phosphate dehydrogenase-derived NADPH.

Item

http://www.wikidata.org/entity/Q37264479

description

article científic

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article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on 08 May 2009

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vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

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name

Superoxide production by NAD

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Superoxide production by NAD(P ...... e dehydrogenase-derived NADPH.

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Superoxide production by NAD

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Superoxide production by NAD(P ...... e dehydrogenase-derived NADPH.

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Superoxide production by NAD

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Superoxide production by NAD(P ...... e dehydrogenase-derived NADPH.

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P1476

Superoxide production by NAD(P ...... e dehydrogenase-derived NADPH.

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P2093

Beverly C Floyd

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Fabio Recchia

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Mark Kozicky

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Michael S Wolin

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Rakhee S Gupte

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Sabrina Serpillon

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Sachin A Gupte

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Shimran George

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Venessa Neito

http://www.w3.org/2001/XMLSchema#string

William Stanley

http://www.w3.org/2001/XMLSchema#string

P2860

Biochemistry and molecular cell biology of diabetic complications

Glucose-6 phosphate dehydrogenase deficiency decreases the vascular response to angiotensin II

NOX enzymes and the biology of reactive oxygen

Mechanisms underlying endothelial dysfunction in diabetes mellitus.

Overexpression of glucose-6-phosphate dehydrogenase is associated with lipid dysregulation and insulin resistance in obesity

Human alpha B-crystallin mutation causes oxido-reductive stress and protein aggregation cardiomyopathy in mice

The coronary circulation in diabetes: influence of reactive oxygen species on K+ channel-mediated vasodilation.

Regulation of endothelial-type NO synthase expression in pathophysiology and in response to drugs.

Cardiac endothelial-myocardial signaling: its role in cardiac growth, contractile performance, and rhythmicity.

Vascular NAD(P)H oxidases: specific features, expression, and regulation.

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10.1152/AJPHEART.01142.2008

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Superoxide production by NAD(P)H oxidase and mitochondria is increased in genetically obese and hyperglycemic rat heart and aorta before the development of cardiac dysfunction. The role of glucose-6-phosphate dehydrogenase-derived NADPH.

about

P2860

P2860

Superoxide production by NAD(P)H oxidase and mitochondria is increased in genetically obese and hyperglycemic rat heart and aorta before the development of cardiac dysfunction. The role of glucose-6-phosphate dehydrogenase-derived NADPH.

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