Aging alters the effect of adiponectin receptor signaling on bone marrow-derived mesenchymal stem cells.

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Tác giả: Pei Hu, Bolun Li, Hanghang Liu, Shibo Liu, Yao Liu, En Luo, Qiucheng Zhao, Zizhuo Zheng

Ngôn ngữ: eng

Ký hiệu phân loại: 912.01 Philosophy and theory

Thông tin xuất bản: England : Aging cell , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 59413

Adiponectin receptor signaling represents a promising therapeutic target for age-related conditions such as osteoporosis and diabetes. However, the literature presents conflicting evidence regarding the role of adiponectin signaling in bone homeostasis and fracture repair across different health states, ages, and disease conditions. These inconsistencies may arise from the complex endocrine and paracrine feedback mechanisms regulating adiponectin, as well as the variability in adiponectin isoforms and receptor expressions. In this study, we observed differential expression of adiponectin receptors in the bone marrow (BM) of aged mice, characterized by elevated levels of adiponectin receptor 2 and reduced levels of receptor 1, as corroborated by both single-cell sequencing and in vivo staining. Additionally, circulating levels of adiponectin and its local expression were significantly higher in aged mice compared to younger counterparts. Treatment with adiponectin receptor agonist, AdipoRon, enhanced bone regeneration and repair in young mice by promoting osteogenesis and reducing osteoclastogenesis. Conversely, in aged mice, AdipoRon treatment led to cellular senescence, delayed bone repair, and inhibited osteogenic activity. Notably, the adiponectin receptor 1-Wnt and adiponectin receptor 2-MAPK and mTOR signaling pathways were differentially activated in AdipoRon-treated BM mesenchymal stem cells from young and aged mice. Additionally, the NF-κB, and AKT pathways were consistently downregulated in BM macrophages of both age groups following AdipoRon administration. In conclusion, aging significantly modulates the impact of adiponectin receptor signaling on BM mesenchymal stem cells. This modulation is potentially attributable to changes in receptor transcription and distribution, as well as differential activation of downstream signaling pathways.
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