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

Jione Kang, Mi Gyeong Jeong, Sera Oh, Eun Jung Jang, Hyo Kyeong Kim, Eun Sook Hwang

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43 Scopus citations


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 languageEnglish
Pages (from-to)79-85
Number of pages7
JournalFEBS Letters
Issue number1
StatePublished - 3 Jan 2014

Bibliographical note

Funding Information:
We thank Dr. J. Alam (Alton Ochsner Medical Foundation, New Orleans) for providing pHO4.3k-luc vector and Ms. Hyun Jung Kim for helping histological analysis. This work was supported by the Basic research program ( 2012R1A1B3000603 for ESH and 2011-007983 for JOK) of the National Research Foundation funded by Ministry of Education, Science, and Technology.


  • FoxO1
  • MAFbx
  • MuRF1
  • NRF2
  • Nerve injury


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