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Peer-reviewedCC BY-NC-ND 4.0Immunity & Ageing : I & A

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

  • Qinfeng Zhou1,2
  • Kaixuan Wang2,3
  • Xiaoxian Sun2,4
  • Jingyue Fu2,5
  • Lei Wang1
  • Qing Wang6
  • Yong Ma2,3,5
  • Yang Guo2,7
7 affiliations
  1. 1Department of Laboratory Medicine, Zhangjiagang TCM Hospital Affiliated to Nanjing University of Chinese Medicine/Zhangjiagang Traditional Chinese Medicine Hospital, Zhangjiagang, Jiangsu 215699 China
  2. 2Laboratory of New Techniques of Restoration & Reconstruction of Orthopedics and Traumatology, Nanjing University of Chinese Medicine, Nanjing, 210023 Jiangsu China
  3. 3School of Integrative Medicine, Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210023 China
  4. 4Department of Trauma and Orthopedics, Wuxi Affiliated Hospital of Nanjing University of Chinese Medicine, Wuxi, Jiangsu 214071 China
  5. 5Yancheng TCM Hospital Affiliated to Nanjing University of Chinese Medicine, Yancheng, Jiangsu 224000 China
  6. 6TCM Nursing Intervention Key Laboratory of Chronic Disease, Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210023 China
  7. 7Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210023 China
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Abstract

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.

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Cite

BibTeXRIS
BibTeX
@article{zhou2026macrophage,
  title = {{Macrophage senescence and senescence-like states in senile osteoporosis: cellular cross-talk and therapeutic perspectives}},
  author = {Qinfeng Zhou and Kaixuan Wang and Xiaoxian Sun and Jingyue Fu and Lei Wang and Qing Wang and Yong Ma and Yang Guo},
  journal = {Immunity \& Ageing : I \& A},
  year = {2026},
  month = jul,
  doi = {10.1186/s12979-026-00586-4},
  url = {https://doi.org/10.1186/s12979-026-00586-4},
  note = {CC BY-NC-ND 4.0},
}
RIS
TY  - JOUR
TI  - Macrophage senescence and senescence-like states in senile osteoporosis: cellular cross-talk and therapeutic perspectives
AU  - Qinfeng Zhou
AU  - Kaixuan Wang
AU  - Xiaoxian Sun
AU  - Jingyue Fu
AU  - Lei Wang
AU  - Qing Wang
AU  - Yong Ma
AU  - Yang Guo
PY  - 2026
DA  - 2026/07/31
JO  - Immunity & Ageing : I & A
DO  - 10.1186/s12979-026-00586-4
UR  - https://doi.org/10.1186/s12979-026-00586-4
AB  - 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.
SN  - 1742-4933
ER  -