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Ultrathin WO x Nanoribbons with Moderate ROS Clearance and Antibacterial Abilities Efficiently Induce M2 Macrophage Polarization for Diabetic Bone Defect Repair

The repair of bone defects in diabetes remains a major challenge in the field of biomedicine because of the disturbance of bone immune homeostasis and the susceptibility of exposed wounds to bacterial infection. Clinically, immunoregulation by removing excessive reactive oxygen species (ROS) effecti...

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Bibliographic Details
Published in:Advanced functional materials 2024-02, Vol.34 (8)
Main Authors: Wang, Jiechen, Zhang, Chenguang, Zhang, Wenshu, Liu, Wenwen, Guo, Yaru, Dang, Pengrui, Wei, Ling, Zhao, Han, Deng, Xuliang, Guo, Shaojun, Chen, Lili
Format: Article
Language:English
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Summary:The repair of bone defects in diabetes remains a major challenge in the field of biomedicine because of the disturbance of bone immune homeostasis and the susceptibility of exposed wounds to bacterial infection. Clinically, immunoregulation by removing excessive reactive oxygen species (ROS) effectively promotes diabetic bone defect repair. However, aggressive ROS clearance can disrupt ROS homeostasis, making ROS‐mediated polarization of M2 macrophages in the process of tissue healing of diabetes be difficult. Herein, an ultrathin defective tungsten oxide (WO x ) nanoribbon with high oxygen vacancies to simultaneously achieve moderate scavenging of ROS and high broad‐spectrum photothermal antibacterial activity to promote diabetic bone defect repair is reported. It is demonstrated that the moderate ROS clearance ability of WO x nanoribbons can remodel metabolic patterns for achieving 86.3% M2 macrophage induction in a high glucose microenvironment. This high induction efficiency combined with excellent photothermal antibacterial ability of WO x nanoribbons markedly alleviated the inflammatory reaction and efficiently facilitated the repair of bone defects infected with methicillin‐resistant Staphylococcus aureus ( S. aureus ) in C57BLKS/J (BKS)‐diabetic (BKS‐db) mice.
ISSN:1616-301X
1616-3028
DOI:10.1002/adfm.202306319