NADPH oxidase hyperactivity induces plantaris atrophy in heart failure rats

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Arquivos
art_BECHARA_NADPH_oxidase_hyperactivity_induces_plantaris_atrophy_in_heart_2014.PDF (1.12 MB)
Citações na Scopus
54
Tipo de produção
article
Data de publicação
2014
DOI
Scopus
Web of Science
Título da Revista
ISSN da Revista
Título do Volume
Editora
ELSEVIER IRELAND LTD
Autores
BECHARA, Luiz R. G.
MOREIRA, Jose B. N.
JANNIG, Paulo R.
VOLTARELLI, Vanessa A.
VASCONCELOS, Andrea R.
SCAVONE, Cristoforo
RAMIRES, Paulo R.
BRUM, Patricia C.
Citação
INTERNATIONAL JOURNAL OF CARDIOLOGY, v.175, n.3, p.499-507, 2014
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
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-kappa B 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-kappa B activity, p38 MAPK phosphorylation and UPS activation. NADPH oxidase inhibition by apocynin prevented MI-induced skeletal muscle atrophy by reducing ROS production, NF-kappa B 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.
Palavras-chave
Heart failure, Skeletal muscle, Oxidative stress, NADPH oxidase, Atrophy
URI
https://observatorio.fm.usp.br/handle/OPI/8730
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Coleções
Artigos e Materiais de Revistas Científicas - HC/InCor