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- W2012300541 abstract "The role of nuclear factor-erythroid 2 p45-related factor 2 (Nrf2) and Kelch-like ECH-associated protein 1 (Keap1) redox signaling has not been characterized in human skeletal muscle despite an extensive delineation of oxidative stress in the etiology of aging and sarcopenia. We assessed whether the age-associated decline in antioxidant response is due, at least in part, to dysfunction in Nrf2-Keap1 redox signaling. We also evaluated whether an active lifestyle can conserve skeletal muscle cellular redox status via activation of Nrf2-Keap1 signaling. Here we show that a recreationally active lifestyle is associated with the activation of upstream modulators that induce the Nrf2-mediated antioxidant response cascade in skeletal muscle of the elderly. Conversely, a sedentary lifestyle is negatively associated with these adaptations mainly because of dysregulation of Nrf2-Keap1 redox signaling that renders the intracellular environment prone to reactive oxygen species-mediated toxicity. Our results indicate that an active lifestyle is an important determinant of cellular redox status. We propose that the metabolic induction of Nrf2-Keap1 redox signaling promises to be a viable therapy for attenuating oxidative stress-mediated damage in skeletal muscle associated with physical inactivity." @default.
- W2012300541 created "2016-06-24" @default.
- W2012300541 creator A5003074930 @default.
- W2012300541 creator A5020091796 @default.
- W2012300541 creator A5039070791 @default.
- W2012300541 date "2010-11-01" @default.
- W2012300541 modified "2023-10-14" @default.
- W2012300541 title "Dysfunctional Nrf2–Keap1 redox signaling in skeletal muscle of the sedentary old" @default.
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- W2012300541 doi "https://doi.org/10.1016/j.freeradbiomed.2010.08.010" @default.
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