title: Left ventricular remodeling after myocardial infarction in mice with targeted deletion of the NADPH oxidase subunit gp91PHOX.
abstract: BACKGROUND
  Oxidative stress is involved in progression of left ventricular hypertrophy and heart failure. Since NADPH oxidases are a major source of reactive oxygen species in the heart, we studied left ventricular remodeling after myocardial infarction in mice with targeted deletion of the NADPH oxidase subunit gp91(phox).
  
  
  RESULTS
  gp91(phox) knockout (KO) and wild-type (WT) animals underwent coronary artery ligation. Mortality was significant higher in the gp91(phox) KO mice. However, transthoracic echocardiography performed at days 1, 7, and 56 at mid-papillary levels revealed that progression of left ventricular remodeling was not influenced by the genotype. Moreover, systemic oxidative stress was not reduced in gp91(phox) KO mice as indicated by a significant increase in lipid peroxides potentially mediated by an increase of the NADPH subunit nox-1 in gp91(phox) KO mice.
  
  
  CONCLUSIONS
  Targeted deletion of the NADPH subunit gp91(phox) does not affect left ventricular remodeling following myocardial infarction and does not decrease the production of oxidative stress. However, the final role of the different NADPH subunits in the heart under pathophysiologic conditions remains to be determined.
authors.affiliation: Medizinische Universitätsklinik Würzburg, Josef-Schneider Str. 2, 97080 Würzburg, Germany. frantz_s@medizin.uni-wuerzburg.de
authors.forename: Stefan
authors.initials: S
authors.lastname: Frantz
authors.forename: Ralf P
authors.initials: RP
authors.lastname: Brandes
authors.forename: Kai
authors.initials: K
authors.lastname: Hu
authors.forename: Konrad
authors.initials: K
authors.lastname: Rammelt
authors.forename: Jürgen
authors.initials: J
authors.lastname: Wolf
authors.forename: Heidi
authors.initials: H
authors.lastname: Scheuermann
authors.forename: Georg
authors.initials: G
authors.lastname: Ertl
authors.forename: Johann
authors.initials: J
authors.lastname: Bauersachs
mesh_terms: D000818:Animals; D004452:Echocardiography; D017353:Gene Deletion; D008562:Membrane Glycoproteins / Q000235:genetics*; D051379:Mice; D018345:Mice, Knockout; D009203:Myocardial Infarction / Q000503:physiopathology*; D000074662:NADPH Oxidase 2; D019255:NADPH Oxidases / Q000235:genetics*; D018384:Oxidative Stress / Q000502:physiology; D020257:Ventricular Remodeling / Q000235:genetics*
chemical_list: D008562:Membrane Glycoproteins; C488842:Cybb protein, mouse; D000074662:NADPH Oxidase 2; D019255:NADPH Oxidases