Protective Effect of Delta-Like 1 Homolog Against Muscular Atrophy in a Mouse Model

Ji Young Lee, Minyoung Lee, Dong Hee Lee, Yong Ho Lee, Byung Wan Lee, Eun Seok Kang, Bong Soo Cha

Research output: Contribution to journalArticlepeer-review


Background: Muscle atrophy is caused by an imbalance between muscle growth and wasting. Delta-like 1 homolog (DLK1), a protein that modulates adipogenesis and muscle development, is a crucial regulator of myogenic programming. Thus, we investigated the effect of exogenous DLK1 on muscular atrophy. Methods: We used muscular atrophy mouse model induced by dexamethasone (Dex). The mice were randomly divided into three groups: (1) control group, (2) Dex-induced muscle atrophy group, and (3) Dex-induced muscle atrophy group treated with DLK1. The effects of DLK1 were also investigated in an in vitro model using C2C12 myotubes. Results: Dex-induced muscular atrophy in mice was associated with increased expression of muscle atrophy markers and decreased expression of muscle differentiation markers, while DLK1 treatment attenuated these degenerative changes together with reduced expression of the muscle growth inhibitor, myostatin. In addition, electron microscopy revealed that DLK1 treatment improved mitochondrial dynamics in the Dex-induced atrophy model. In the in vitro model of muscle atrophy, normalized expression of muscle differentiation markers by DLK1 treatment was mitigated by myostatin knockdown, implying that DLK1 attenuates muscle atrophy through the myostatin pathway. Conclusion: DLK1 treatment inhibited muscular atrophy by suppressing myostatin-driven signaling and improving mitochondrial biogenesis. Thus, DLK1 might be a promising candidate to treat sarcopenia, characterized by muscle atrophy and degeneration.

Original languageEnglish
Pages (from-to)684-697
Number of pages14
JournalEndocrinology and Metabolism
Issue number4
Publication statusPublished - 2022 Aug

Bibliographical note

Funding Information:
This study was partly supported by research fund from Dong-A ST Research Center, 2015−2018 (grant No RM0170). The funder had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. This article is based in part on the previously published PhD thesis of Ji Young Lee.

Publisher Copyright:
Copyright © 2022 Korean Endocrine Society.

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology


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