The research and application of bone-targeted engineered exosomes and the bone microenvironment represent an interdisciplinary cutting-edge hotspot. Its primary goal is to use biomimetic nanomaterials as drug carriers to achieve targeted drug delivery, controlled release, and enhanced therapeutic efficacy by regulating their interactions with bone tissue cells, immune cells, bone marrow stroma and other components.


Targeted nanomedicines are adopted to achieve precise bone targeting and immune evasion. This composite nanomedicine consists of drug-loaded metal-organic frameworks (ZIF-8) coated with mesenchymal stem cell exosomes (MSC-Exos) co-expressing CXCR4 and CD47. Once this nanosystem enters the blood circulation, the CD47 protein on its surface can effectively avoid phagocytosis by the mononuclear phagocyte system. Upon reaching the bone marrow microenvironment, CXCR4 on the exosome surface specifically recognizes and binds to stromal cell-derived factor 1α (SDF-1α), guiding the precise enrichment of the nanomedicine in bone tissue and reducing non-specific distribution.


An acid-responsive release mechanism is utilized to remodel the bone microenvironment and promote osteogenesis. This nanomedicine is composed of an acid-sensitive ZIF-8 core and a biomembrane shell. When the complex enters the acidic pathological microenvironment of osteoporosis, the ZIF-8 framework disintegrates and simultaneously releases betaine and zinc ions. Betaine specifically binds to cytoplasmic 14-3-3 protein, triggering dephosphorylation of TFEB at key sites and its subsequent nuclear translocation, which activates the autophagy-lysosome signaling network. This reverses the senescent phenotype of bone marrow mesenchymal stem cells (BMSCs) and restores their osteogenic differentiation potential.

The synergistic regulatory function of the nanoplatform is harnessed to re-establish bone metabolic homeostasis. This nanomedicine is constructed as a betaine-loaded MOF-exosome hybrid system. It exerts multi-target synergistic effects within the complex bone metabolic microenvironment. The released zinc ions block the NF-κB pathway, inhibit RANKL-induced osteoclast differentiation and maturation, and attenuate pathological bone resorption. Combined with betaine-mediated osteogenic activation, it achieves bidirectional regulation by both promoting bone formation and suppressing bone resorption, thereby effectively correcting pathological bone loss.

We provide full-process services for various material design, including highly innovative scheme design, preparation, characterization, and in vitro & in vivo validation (cell/animal experiments). Our postdoctoral team, with multiple high-impact Q1 publications, can tackle your challenging and sophisticated research demands. Our scope covers hydrogels, drug delivery, nanomaterials, polymers, liposomes, microneedle drug delivery and more. We support project design, National Natural Science Foundation application, and the publication of high-impact Q1/Q2 papers in journals such as AFM, SCI and AM. Feel free to reach out👇️
17768014569 (Senior Engineer)
17761925168 (Engineer Zhang)
18013729810 (Engineer Yang)