Ago, Tetsuro <br/><br/>
Upregulation of Nox4 by hypertrophic stimuli promotes apoptosis and mitochondrial dysfunction in cardiac myocytes.  [electronic resource] 

 -  Circulation research  Apr 2010 
 - 1253-64 p.  digital 
<br/><br/> Publication Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. 
<br/><br/><label>ISSN: </label>1524-4571 
<br/><br/><label>Standard No.: </label>10.1161/CIRCRESAHA.109.213116  doi 
<br/><br/><label>Subjects--Topical Terms: </label><br/>Aconitate Hydratase--metabolism<br/>Aging--metabolism<br/>Animals<br/>Apoptosis--drug effects<br/>Cardiomegaly--enzymology<br/>Cell Proliferation<br/>Cells, Cultured<br/>Cysteine<br/>Disease Models, Animal<br/>Enzyme Inhibitors--pharmacology<br/>Fibrosis<br/>Genotype<br/>Humans<br/>Mice<br/>Mice, Transgenic<br/>Mitochondria, Heart--drug effects<br/>Myocytes, Cardiac--drug effects<br/>NADH Dehydrogenase--metabolism<br/>NADPH Oxidase 4<br/>NADPH Oxidases--antagonists & inhibitors<br/>Onium Compounds--pharmacology<br/>Oxidation-Reduction<br/>Oxidative Stress<br/>Phenotype<br/>Rats<br/>Rats, Wistar<br/>Rotenone--pharmacology<br/>Superoxides--metabolism<br/>Transfection<br/>Uncoupling Agents--pharmacology<br/>Up-Regulation<br/>Ventricular Dysfunction, Left--enzymology<br/>Ventricular Function, Left