骨髓
线粒体
细胞生物学
氧化磷酸化
骨重建
炎症
间充质干细胞
活性氧
癌症研究
生物
细胞凋亡
转录组
重编程
氧化应激
骨质疏松症
干细胞
新陈代谢
线粒体分裂
细胞内
细胞外
成骨细胞
骨髓干细胞
骨组织
骨细胞
间质细胞
程序性细胞死亡
作者
Di Wang,Da Zhong,Yizhe He,Jialiang Xie,Dong Ruan,Liwen Liu,Zhibo Tang,Weichang Xie,Jun Luo,Mingchuan Yu
标识
DOI:10.1002/adma.202521645
摘要
Osteoporosis is characterized by impaired bone formation and disrupted bone marrow homeostasis, largely driven by mitochondrial dysfunction in bone marrow mesenchymal stem cells (BMSCs). To address this, a live mitochondrial delivery system composed of CXCR4-engineered macrophages loaded with nanozyme-functionalized mitochondria (CM-MTBM). This system integrates bone-targeted migration, reactive oxygen species scavenging, and communication-mediated mitochondrial transfer. CM-MTBM restores mitochondrial respiration, enhances osteogenic differentiation, and alleviates oxidative apoptosis in BMSCs, thereby promoting metabolic recovery and redox balance. In osteoporotic mice, CM-MTBM treatment markedly improved the trabecular bone microarchitecture and promoted osteogenic repair. Single-cell transcriptomic analysis further revealed the enrichment of osteogenic BMSC subpopulations and functional reprogramming of the bone marrow immune-metabolic microenvironment. Mechanistically, CM-MTBM activated mitochondrial oxidative metabolism while suppressing inflammation and senescence-associated signaling, achieving coordinated metabolic and osteogenic activation. Collectively, this work established a communication-driven mitochondrial transfer paradigm that reframes mitochondrial therapy from passive structural supplementation to communication-driven metabolic reprogramming, establishing a conceptual and technological framework for precision treatment of metabolic bone disorders.
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