镁促进OVX大鼠肩袖撕裂修复及缓解干细胞衰老作用。

IF 3.3 3区生物学 Q3 CELL BIOLOGY

Experimental cell research Pub Date : 2025-05-08 DOI:10.1016/j.yexcr.2025.114593

Minghui Sun , Weijiao Zhang , Xin Sun , Kaixu Yu , Xiangming He , Liming Zheng , Ziao Ling , Kaikai Duan , Xiling Qi , Yan Liu , Xin Zhao , Hui Wang , Jiankun Xu , Yifeng Zhang

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引用次数: 0

摘要

骨质疏松症患者术后肌腱-骨交界处（en这些）肌腱袖撕裂（RCT）修复主要受到肱骨结节区受损骨形成不良的阻碍。我们发现，长期口服镁离子（Mg2+）可以显著促进卵巢切除（OVX）大鼠RCT术后肱骨结节骨形成和再生，这是由于Mg2+对骨髓间充质干细胞（BMSCs）的成骨分化有促进作用，并抑制新骨矿化。同时，Mg2+可显著缓解骨髓间充质干细胞的体外复制衰老标志物。BMSCs的RNA-seq数据分析和细胞能量代谢结果表明，Mg2+显著增加衰老BMSCs的线粒体跨膜电位和细胞内ATP含量，减少活性氧的产生。

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Magnesium promoting OVX rats’ rotator cuff tear repair with relieving stem cell senescence effect

The rotator cuff tear (RCT) repairing of tendon-to-bone junction (enthese) after surgery in osteoporotic patients is mainly hindered by poor bone formation at the damaged humeral tuberosity region. We found that long-term oral supplementation of Magnesium ions (Mg²⁺) can significantly promote humeral tuberosity bone formation and enthese regeneration after RCT surgery in ovariectomized (OVX) rats, attributing to the promotive effect of Mg²⁺ on the osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) and its inhibition of new bone mineralization. Meanwhile, the in vitro replicative senescent markers of BMSCs are significantly relieved by Mg²⁺. The BMSCs' RNA-seq data analysis and cell energy metabolism results indicate that Mg²⁺ significantly increase senescent BMSCs’ mitochondrial transmembrane potential and intracellular ATP content, and reduce reactive oxygen species production.

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来源期刊

Experimental cell research 医学-细胞生物学

CiteScore

7.20

自引率

0.00%

发文量

295

审稿时长

30 days

期刊介绍： Our scope includes but is not limited to areas such as: Chromosome biology; Chromatin and epigenetics; DNA repair; Gene regulation; Nuclear import-export; RNA processing; Non-coding RNAs; Organelle biology; The cytoskeleton; Intracellular trafficking; Cell-cell and cell-matrix interactions; Cell motility and migration; Cell proliferation; Cellular differentiation; Signal transduction; Programmed cell death.