Rapamycin reduces severity of senile osteoporosis by activating osteocyte autophagy

D Luo1, H Ren2, T Li1

  • 1Department of Orthopaedic Surgery, Orthopaedic Center of People's Liberation Army, The Affiliated Southeast Hospital of Xiamen University, Zhangzhou, 363000, China.

Abstract

Insights

Rapamycin treatment in old male rats improved bone density and microstructure by activating osteocyte autophagy. This intervention reduced bone loss and osteocyte apoptosis, suggesting a potential therapy for senile osteoporosis.

Area of Science:

  • Bone Biology
  • Cellular Aging
  • Pharmacology

Background:

  • Osteocytes orchestrate bone remodeling; their declining autophagy contributes to senile osteoporosis.
  • Autophagy is crucial for osteocyte viability, and its age-related failure is linked to osteoporosis.

Purpose of the Study:

  • To investigate the protective effects of rapamycin, an autophagy activator, on senile osteoporosis.
  • To determine if rapamycin induces osteocyte autophagy and mitigates age-related bone deterioration.

Main Methods:

  • Old male rats received rapamycin or vehicle control for 12 weeks.
  • Bone mineral density, microstructure, mineral apposition rate, and osteoclast number were assessed.
  • Osteocyte autophagy, apoptosis, and bone turnover markers were analyzed.

Main Results:

  • Rapamycin treatment preserved trabecular bone structure and increased bone mineral density.
  • Rapamycin enhanced mineral apposition rate and reduced osteoclast numbers.
  • Increased autophagy markers (LC3) and reduced osteocyte apoptosis were observed in rapamycin-treated rats.

Conclusions:

  • Rapamycin partially ameliorates age-related bone changes in male rats by activating osteocyte autophagy.
  • The findings suggest rapamycin as a potential therapeutic strategy for senile osteoporosis.

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