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Exercise training prevents oxidative stress and ubiquitin-proteasome system overactivity and reverse skeletal muscle atrophy in heart failure.

Telma F Cunha | Aline V N Bacurau | Jose B N Moreira | Nathalie A Paixão | Juliane C Campos | Julio C B Ferreira | Marcelo L Leal | Carlos E Negrão | Anselmo S Moriscot | Ulrik Wisløff | Patricia C Brum
PloS one | 2012

Heart failure (HF) is known to lead to skeletal muscle atrophy and dysfunction. However, intracellular mechanisms underlying HF-induced myopathy are not fully understood. We hypothesized that HF would increase oxidative stress and ubiquitin-proteasome system (UPS) activation in skeletal muscle of sympathetic hyperactivity mouse model. We also tested the hypothesis that aerobic exercise training (AET) would reestablish UPS activation in mice and human HF.

Pubmed ID: 22870245

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C57BL/6J (tool)

RRID:IMSR_JAX:000664

Mus musculus with name C57BL/6J from IMSR.

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