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FEBS Lett. 2014 Jan 3;588(1):79-85. doi: 10.1016/j.febslet.2013.11.009. Epub 2013 Nov 20.

A FoxO1-dependent, but NRF2-independent induction of heme oxygenase-1 during muscle atrophy.

Author information

  • 1College of Pharmacy and Global Top5 Research Program, Ewha Womans University, Seoul 120-750, Republic of Korea.
  • 2College of Pharmacy and Global Top5 Research Program, Ewha Womans University, Seoul 120-750, Republic of Korea. Electronic address: eshwang@ewha.ac.kr.

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.

KEYWORDS:

FoxO1; MAFbx; MuRF1; NRF2; Nerve injury

PMID:
24269680
DOI:
10.1016/j.febslet.2013.11.009
[PubMed - indexed for MEDLINE]
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