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

Research output: Contribution to journalArticlepeer-review

40 Scopus citations

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 languageEnglish
Pages (from-to)79-85
Number of pages7
JournalFEBS Letters
Volume588
Issue number1
DOIs
StatePublished - 3 Jan 2014

Keywords

  • FoxO1
  • MAFbx
  • MuRF1
  • NRF2
  • Nerve injury

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