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Dkk3 dependent transcriptional regulation controls age related skeletal muscle atrophy

Author

Listed:
  • Jie Yin

    (Chinese Academy of Sciences
    University of Chinese Academy of Sciences)

  • Lele Yang

    (Chinese Academy of Sciences
    University of Chinese Academy of Sciences)

  • Yangli Xie

    (The Third Military Medical University)

  • Yan Liu

    (Chinese Academy of Sciences)

  • Sheng Li

    (Chinese Academy of Sciences)

  • Wenjun Yang

    (Chinese Academy of Sciences)

  • Bo Xu

    (Chinese Academy of Sciences
    University of Chinese Academy of Sciences)

  • Hongbin Ji

    (Chinese Academy of Sciences)

  • Lianghua Ding

    (Soochow University)

  • Kun Wang

    (Soochow University)

  • Gang Li

    (Tongji University School of Medicine)

  • Lin Chen

    (The Third Military Medical University)

  • Ping Hu

    (Chinese Academy of Sciences
    University of Chinese Academy of Sciences)

Abstract

Age-related muscle atrophy (sarcopenia) is the leading cause for disability in aged population, but the underlying molecular mechanisms are poorly understood. Here we identify a novel role for the secreted glycoprotein Dickkopf 3 (Dkk3) in sarcopenia. Forced expression of Dkk3 in muscles in young mice leads to muscle atrophy. Conversely, reducing its expression in old muscles restores both muscle size and function. Dkk3 induces nuclear import of β-catenin and enhances its interaction with FoxO3, which in turn activates the transcription of E3 ubiquitin ligase Fbxo32 and Trim63, driving muscle atrophy. These findings suggest that Dkk3 may be used as diagnostic marker and as therapeutic target for age-related muscle atrophy, and reveal a distinct transcriptional control of Fbxo32 and Trim63.

Suggested Citation

  • Jie Yin & Lele Yang & Yangli Xie & Yan Liu & Sheng Li & Wenjun Yang & Bo Xu & Hongbin Ji & Lianghua Ding & Kun Wang & Gang Li & Lin Chen & Ping Hu, 2018. "Dkk3 dependent transcriptional regulation controls age related skeletal muscle atrophy," Nature Communications, Nature, vol. 9(1), pages 1-13, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-04038-6
    DOI: 10.1038/s41467-018-04038-6
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