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NADPH oxidase hyperactivity induces plantaris atrophy in heart failure rats.
Bechara, Luiz R G; Moreira, Jose B N; Jannig, Paulo R; Voltarelli, Vanessa A; Dourado, Paulo M; Vasconcelos, Andrea R; Scavone, Cristoforo; Ramires, Paulo R; Brum, Patricia C.
Afiliação
  • Bechara LR; School of Physical Education and Sport, University of Sao Paulo, Brazil.
  • Moreira JB; School of Physical Education and Sport, University of Sao Paulo, Brazil; K.G. Jebsen Center of Exercise in Medicine, Norwegian University of Science and Technology (NTNU), Trondheim, Norway.
  • Jannig PR; School of Physical Education and Sport, University of Sao Paulo, Brazil.
  • Voltarelli VA; School of Physical Education and Sport, University of Sao Paulo, Brazil.
  • Dourado PM; Heart Institute, Faculty of Medicine, University of Sao Paulo, Brazil.
  • Vasconcelos AR; Department of Pharmacology, Institute of Biomedical Science, University of São Paulo, Brazil.
  • Scavone C; Department of Pharmacology, Institute of Biomedical Science, University of São Paulo, Brazil.
  • Ramires PR; School of Physical Education and Sport, University of Sao Paulo, Brazil.
  • Brum PC; School of Physical Education and Sport, University of Sao Paulo, Brazil. Electronic address: pcbrum@usp.br.
Int J Cardiol ; 175(3): 499-507, 2014 Aug 20.
Article em En | MEDLINE | ID: mdl-25023789
BACKGROUND: Skeletal muscle wasting is associated with poor prognosis and increased mortality in heart failure (HF) patients. Glycolytic muscles are more susceptible to catabolic wasting than oxidative ones. This is particularly important in HF since glycolytic muscle wasting is associated with increased levels of reactive oxygen species (ROS). However, the main ROS sources involved in muscle redox imbalance in HF have not been characterized. Therefore, we hypothesized that NADPH oxidases would be hyperactivated in the plantaris muscle of infarcted rats, contributing to oxidative stress and hyperactivation of the ubiquitin-proteasome system (UPS), ultimately leading to atrophy. METHODS: Rats were submitted to myocardial infarction (MI) or Sham surgery. Four weeks after surgery, MI and Sham groups underwent eight weeks of treatment with apocynin, a NADPH oxidase inhibitor, or placebo. NADPH oxidase activity, oxidative stress markers, NF-κB activity, p38 MAPK phosphorylation, mRNA and sarcolemmal protein levels of NADPH oxidase components, UPS activation and fiber cross-sectional area were assessed in the plantaris muscle. RESULTS: The plantaris of MI rats displayed atrophy associated with increased Nox2 mRNA and sarcolemmal protein levels, NADPH oxidase activity, ROS production, lipid hydroperoxides levels, NF-κB activity, p38 MAPK phosphorylation and UPS activation. NADPH oxidase inhibition by apocynin prevented MI-induced skeletal muscle atrophy by reducing ROS production, NF-κB hyperactivation, p38 MAPK phosphorylation and proteasomal hyperactivity. CONCLUSION: Our data provide evidence for NADPH oxidase hyperactivation as an important source of ROS production leading to plantaris atrophy in heart failure rats, suggesting that this enzyme complex plays key role in skeletal muscle wasting in HF.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Glicoproteínas de Membrana / Atrofia Muscular / Músculo Esquelético / NADPH Oxidases / Insuficiência Cardíaca Limite: Animals Idioma: En Revista: Int J Cardiol Ano de publicação: 2014 Tipo de documento: Article País de afiliação: Brasil País de publicação: Holanda
Texto completo
Adicionar na Minha BVS
Imprimir
XML
PubMed Links
Buscar no Google

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Glicoproteínas de Membrana / Atrofia Muscular / Músculo Esquelético / NADPH Oxidases / Insuficiência Cardíaca Limite: Animals Idioma: En Revista: Int J Cardiol Ano de publicação: 2014 Tipo de documento: Article País de afiliação: Brasil País de publicação: Holanda