文献类型：期刊文献

英文题名：Irisin reshapes bone metabolic homeostasis to delay age-related osteoporosis by regulating the multipotent differentiation of BMSCs via Wnt pathway

作者：Xing, Shangman[1];Ma, Yifan[2];Song, Bing[1,3];Bai, Min[4];Wang, Kexin[1];Song, Wenjing[1];Cao, Tingting[1];Guo, Chao[3];Zhang, Yanying[3];Wang, Zhandong[5];Wang, Yongfeng[1,6]

第一作者：Xing, Shangman

通信作者：Wang, YF[1];Wang, ZD[2];Wang, YF[3]

机构：[1]Gansu Univ Chinese Med, Clin Med Coll 1, Lanzhou, Peoples R China;[2]Fourth Mil Med Univ, Lab Anim Ctr, Div Canc Biol, Xian, Peoples R China;[3]Gansu Univ Chinese Med, Med Res & Expt Ctr, Lanzhou, Peoples R China;[4]Ningxia Med Univ, Coll Tradit Chinese Med, Yinchuan, Peoples R China;[5]Gansu Univ Chinese Med, Clin Coll Integrated Tradit Chinese & Western Med, Lanzhou, Peoples R China;[6]Gansu Med Univ, Sch Basic Med, Pingliang, Peoples R China

第一机构：甘肃中医药大学

通信机构：[1]corresponding author), Gansu Univ Chinese Med, Clin Med Coll 1, Lanzhou, Peoples R China;[2]corresponding author), Gansu Univ Chinese Med, Clin Coll Integrated Tradit Chinese & Western Med, Lanzhou, Peoples R China;[3]corresponding author), Gansu Med Univ, Sch Basic Med, Pingliang, Peoples R China.|[10735]甘肃中医药大学;

年份：2025

卷号：11

外文期刊名：FRONTIERS IN MOLECULAR BIOSCIENCES

收录：;WOS:【SCI-EXPANDED(收录号:WOS:001399889400001)】；

基金：The author(s) declare that financial support was received for the research, authorship, and/or publication of this article. This research was supported by the National Natural Science Foundation of China (No. 82360898), the Natural Science Foundation of Gansu Province (No. 24JRRA565), the Science and Technology Program of Gansu Province (No. 23YFFA0068), the Science and Technology Achievement Trans-formation and Cultivation Project of Gansu University of Traditional Chinese Medicine (No. 2023CGZH-21), the Innovation Fund of Gansu University Teachers (No. 2023A-080), Gansu Province Pingliang City Key Research and Development Program Project (No. PL-STK-2024A-031), and Gansu Province Higher Education Teacher Innovation Fund Project (No. 2025A-108).

语种：英文

外文关键词：aging; BMSCs; irisin; age-related osteoporosis; bone-fat balance

摘要：Introduction Bone aging is linked to changes in the lineage differentiation of bone marrow stem cells (BMSCs), which show a heightened tendency to differentiate into adipocytes instead of osteoblasts. The therapeutic potential of irisin in addressing age-related diseases has garnered significant attention. More significantly, irisin has the capacity to enhance bone mass recovery and sustain overall bone health. Its mechanism of action in preventing osteoporosis has generated considerable interest within the research community. Nonetheless, the targeting effect of irisin on age-related osteoporosis and its underlying molecular biological mechanisms remain unclear.Methods The specific role of irisin in osteogenic-adipogenic differentiation in young or aging BMSCs was evaluated by multiple cells staining and quantitative real-time PCR (RT-qPCR) analysis. RNA-seq and protein Western blotting excavated and validated the key pathway by which irisin influences the fate determination of aging BMSCs. The macroscopic and microscopic changes of bone tissue in aging mice were examined using Micro-computed tomography (Micro-CT) and morphological staining.Results It was noted that irisin affected the multilineage differentiation of BMSCs in a manner dependent on the dosage. Simultaneously, the Wnt signaling pathway might be a crucial mechanism through which irisin sustains the bone-fat balance in aging BMSCs and mitigates the decline in pluripotency. In vivo, irisin reduced bone marrow fat deposition in aging mice and effectively alleviating the occurrence of bone loss.Conclusion Irisin mediates the Wnt signaling pathway, thereby influencing the fate determination of BMSCs. In addition, it is essential for preserving metabolic equilibrium in the bone marrow microenvironment and significantly contributes to overall bone health. The findings provide new evidence for the use of iris extract in the treatment of age-related osteoporosis.