Upregulation of Nox4 by hypertrophic stimuli promotes apoptosis and mitochondrial dysfunction in cardiac myocytes. [electronic resource]
Producer: 20100430Description: 1253-64 p. digitalISSN:- 1524-4571
- Aconitate Hydratase -- metabolism
- Aging -- metabolism
- Animals
- Apoptosis -- drug effects
- Cardiomegaly -- enzymology
- Cell Proliferation
- Cells, Cultured
- Cysteine
- Disease Models, Animal
- Enzyme Inhibitors -- pharmacology
- Fibrosis
- Genotype
- Humans
- Mice
- Mice, Transgenic
- Mitochondria, Heart -- drug effects
- Myocytes, Cardiac -- drug effects
- NADH Dehydrogenase -- metabolism
- NADPH Oxidase 4
- NADPH Oxidases -- antagonists & inhibitors
- Onium Compounds -- pharmacology
- Oxidation-Reduction
- Oxidative Stress
- Phenotype
- Rats
- Rats, Wistar
- Rotenone -- pharmacology
- Superoxides -- metabolism
- Transfection
- Uncoupling Agents -- pharmacology
- Up-Regulation
- Ventricular Dysfunction, Left -- enzymology
- Ventricular Function, Left
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Publication Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
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