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Testosterone Delays Bone Microstructural Destruction via Osteoblast-Androgen Receptor-Mediated Upregulation of

Yong Xie1,2,3, Meng Pan2, Zeyuan Zhang1,3

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Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
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Low testosterone levels in elderly men are linked to bone loss and increased fracture risk. The testosterone-androgen receptor-tenascin-C pathway regulates bone remodeling, offering new targets for preventing bone destruction.

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Area of Science:

  • Endocrinology
  • Bone Biology
  • Gerontology

Background:

  • Bone loss and microstructural deterioration in elderly men increase fracture risk and mortality.
  • The protective role of testosterone (Tes) in bone remodeling is established, but its precise regulatory mechanism remains unclear.
  • Elderly men show reduced bone thickness and increased porosity, particularly in the femoral head.

Purpose of the Study:

  • To elucidate the mechanism by which testosterone regulates bone remodeling in elderly men.
  • To identify biomarkers for bone loss associated with low testosterone.
  • To explore potential therapeutic targets for male osteoporosis.

Main Methods:

  • Bone microarchitectural analysis in elderly men and tail-suspended mice.
  • Serum profiling of 352 individuals to correlate testosterone levels with bone loss.
  • In vivo studies using osteoblast-specific androgen receptor knockout mice.
  • Molecular docking to investigate protein interactions.
  • Administration of a synthetic peptide (pep2) in mouse models.

Main Results:

  • Low testosterone levels (<9.415 nmol·L⁻¹) are associated with higher risk of bone loss in elderly men.
  • Mice lacking osteoblastic androgen receptor (AR) exhibited deteriorated femoral bone structure, mirroring human findings.
  • Testosterone enhances osteoblastic differentiation via AR-mediated upregulation of tenascin-C (TNC).
  • TNC's C-terminal domain inhibits osteoclastogenesis by binding integrin αV.
  • A synthetic peptide (pep2) mimicking TNC's domain preserved bone architecture in AR-deficient mice.
  • Elevated serum extracellular vesicle amyloid precursor protein, combined with low testosterone, serves as a biomarker for bone loss.

Conclusions:

  • The testosterone-AR-TNC axis is a critical regulator of bone remodeling in men.
  • This pathway offers novel insights into fracture risk assessment and potential therapeutic interventions for bone destruction.
  • Targeting the Tes-AR-TNC pathway may help prevent bone loss and fractures in aging men.