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Updated: Aug 6, 2025

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Splicing factor YBX1 regulates bone marrow stromal cell fate during aging.

Ye Xiao1, Guang-Ping Cai1, Xu Feng1

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The EMBO Journal
|March 21, 2023
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Summary

Cellular senescence and impaired bone marrow stromal cell (BMSC) differentiation cause age-related bone loss. This study reveals Y-box binding protein 1 (YBX1) loss drives BMSC aging and osteoporosis, with a compound showing therapeutic potential.

Keywords:
Y-box binding protein 1agingalternative splicingbone marrow stromal cells

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Area of Science:

  • Biochemistry
  • Cell Biology
  • Gerontology

Background:

  • Cellular senescence and altered differentiation of bone marrow stromal cells (BMSCs) contribute to age-related bone loss.
  • Alternative splicing (AS) is a key posttranscriptional regulatory pathway influencing gene expression and cellular senescence.

Purpose of the Study:

  • To investigate the role of splicing factors, specifically Y-box binding protein 1 (YBX1), in BMSCs during aging.
  • To explore the therapeutic potential of targeting YBX1 for age-related bone loss.

Main Methods:

  • Examined YBX1 expression in aging BMSCs from mice and humans.
  • Assessed the impact of YBX1 deficiency and overexpression on BMSC senescence and osteogenic differentiation.
  • Investigated the effect of sciadopitysin on YBX1 levels and bone loss in aged mice.

Main Results:

  • YBX1 expression decreased with age in BMSCs.
  • YBX1 deficiency led to mis-splicing of key genes, promoting BMSC senescence and impairing differentiation.
  • Ybx1 deletion accelerated bone loss, while overexpression enhanced bone formation.
  • The compound sciadopitysin protected YBX1 from degradation and reduced bone loss in aged mice.

Conclusions:

  • YBX1 is crucial for maintaining BMSC function and fate through precise RNA splicing control.
  • YBX1 deficiency contributes significantly to age-related osteoporosis.
  • Targeting YBX1 degradation presents a promising therapeutic strategy for osteoporosis.