Abstract
Skeletal muscle plays key roles in metabolic homeostasis. Loss of muscle mass, called muscle atrophy exacerbates disease-associated metabolic perturbations. In this study, we characterized the molecular functions and mechanisms underlying regulation of skeletal muscle atrophy induced by denervation. Denervation significantly increased the expression of heme oxygenase-1 (HO-1) and atrogenes in skeletal muscle. Forkhead box protein O1 (FoxO1) drastically increased in atrophied muscle and selectively stimulated HO-1 gene transcription through direct DNA binding. Lack of HO-1 substantially attenuated muscle atrophy, whereas HO-1 overexpression caused muscle damage in vitro and in vivo. Collectively, HO-1 induced by FoxO1 may cause skeletal muscle atrophy.
Original language | English |
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Pages (from-to) | 79-85 |
Number of pages | 7 |
Journal | FEBS Letters |
Volume | 588 |
Issue number | 1 |
DOIs | |
State | Published - 3 Jan 2014 |
Keywords
- FoxO1
- MAFbx
- MuRF1
- NRF2
- Nerve injury