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Volumn 129, Issue 7, 2015, Pages 561-574

Impaired mitochondrial energy supply coupled to increased H2O2 emission under energy/redox stress leads to myocardial dysfunction during Type I diabetes

Author keywords

Adrenergic stimulation; Calcium transient; Contractility; Diabetes; Energetic transitions; Glutathione; Hyperglycaemia; Redox balance

Indexed keywords

ADENOSINE DIPHOSPHATE; CATALASE; CYTOCHROME C OXIDASE; FATTY ACID; GLUCOSE; GLUTAMIC ACID; GLUTATHIONE; GLUTATHIONE PEROXIDASE; HYDROGEN PEROXIDE; INSULIN; INSULIN GLARGINE; ISOPRENALINE; NICOTINAMIDE ADENINE DINUCLEOTIDE (PHOSPHATE) TRANSHYDROGENASE; OXIDIZING AGENT; OXYGEN; PALMITIC ACID; PEROXIREDOXIN; REACTIVE OXYGEN METABOLITE; STREPTOZOCIN; SUCCINATE DEHYDROGENASE (UBIQUINONE); SUPEROXIDE DISMUTASE; THIOREDOXIN 1; THIOREDOXIN 2; THIOREDOXIN REDUCTASE 1; THIOREDOXIN REDUCTASE 2; BETA ADRENERGIC RECEPTOR; CALCIUM; GLUCOSE BLOOD LEVEL;

EID: 84942932965     PISSN: 01435221     EISSN: 14708736     Source Type: Journal    
DOI: 10.1042/CS20150204     Document Type: Article
Times cited : (29)

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