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<p>Senile osteoporosis (SOP) is an age-related metabolic bone disease characterized by reduced bone quality and increased fracture risk, closely associated with immune senescence. Among immune components in the bone marrow niche, macrophages undergo age-associated phenotypic and functional changes that may impair bone homeostasis; however, whether these changes reflect bona fide senescence, inflammatory activation, or polarization remains unclear. This review summarizes the biological characteristics of senescent macrophages, including alterations in senescence markers, senescence-associated secretory phenotype (SASP), epigenetic modifications, and telomere dynamics. It then outlines their functional changes, focusing on oxidative stress, autophagy, and metabolic dysregulation. Importantly, we discuss how senescent or senescence-like macrophage states may regulate macrophage–bone marrow mesenchymal stem cell (BMSC) crosstalk through SASP-related factors, the grancalcin–plexin-B2 axis, mitochondrial transfer, exosome-mediated signaling, and metabolic reprogramming, while distinguishing direct ageing-related evidence from indirect mechanistic evidence.</p>

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Macrophage senescence and senescence-like states in senile osteoporosis: cellular cross-talk and therapeutic perspectives

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年7月31日

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  • Qinfeng Zhou,
  • Kaixuan Wang,
  • Xiaoxian Sun,
  • Jingyue Fu,
  • Lei Wang,
  • Qing Wang,
  • Yong Ma,
  • Yang Guo

摘要

Senile osteoporosis (SOP) is an age-related metabolic bone disease characterized by reduced bone quality and increased fracture risk, closely associated with immune senescence. Among immune components in the bone marrow niche, macrophages undergo age-associated phenotypic and functional changes that may impair bone homeostasis; however, whether these changes reflect bona fide senescence, inflammatory activation, or polarization remains unclear. This review summarizes the biological characteristics of senescent macrophages, including alterations in senescence markers, senescence-associated secretory phenotype (SASP), epigenetic modifications, and telomere dynamics. It then outlines their functional changes, focusing on oxidative stress, autophagy, and metabolic dysregulation. Importantly, we discuss how senescent or senescence-like macrophage states may regulate macrophage–bone marrow mesenchymal stem cell (BMSC) crosstalk through SASP-related factors, the grancalcin–plexin-B2 axis, mitochondrial transfer, exosome-mediated signaling, and metabolic reprogramming, while distinguishing direct ageing-related evidence from indirect mechanistic evidence.