Intercellular Communication‐Driven Mitochondrial Transfer via CXCR4‐Engineered Macrophages Reprograms Bone Marrow Metabolism for Osteoporosis Therapy

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Authors: Di Wang, Da Zhong, Yizhe He, Jialiang Xie, Dong Ruan, Liwen Liu, Zhibo Tang, Weichang Xie, Jun Luo, Mingchuan Yu
Cited by: 4
References: 36

Abstract

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.

Fields of Study & Subjects

Advanced Nanomaterials in Catalysis Cancer Hypoxia and Metabolism Immune cells in cancer

Publication details

Journal / source
Advanced Materials
Publisher
Wiley
Volume
38
Issue
15
Pages
e21645–e21645
Publication date
7 February 2026
Language
EN