Dkk3 dependent transcriptional regulation controls age related skeletal muscle atrophy

Jie Yin, Lele Yang, Yangli Xie, Yan Liu, Sheng Li, Wenjun Yang, Bo Xu, Hongbin Ji, Lianghua Ding, Kun Wang, Gang Li, Lin Chen and Ping Hu ()
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Jie Yin: Chinese Academy of Sciences
Lele Yang: 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
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

Nature Communications, 2018, vol. 9, issue 1, 1-13

Abstract: 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.

Date: 2018
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DOI: 10.1038/s41467-018-04038-6

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