PhD Student The Chinese University of Hong Kong (CUHK) Hong Kong, China (People's Republic)
Abstract: Bone defects, including structural and functional abnormalities affecting the integrity of bones, represent a significant global health concern. These defects are a key factor in the elevated rates of disability observed globally, underscoring their significant impact on global health. Critical-sized bone defects (CSBDs) are defined as bone defects that are not expected to heal without secondary (surgical) intervention. Skeletal stem/progenitor cells (SSCs) play essential roles in the regeneration of CSBDs and have been enthusiastically pursued in bone tissue engineering. Modulating the metabolic pathway represents an effective strategy to enhance the osteogenic differentiation of SSCs. However, this process is hindered at bone defect sites. The objective of this study was to develop a mitochondria-targeting, single-atom nanozyme to promote the osteogenic differentiation C3H/10T1/2 SSCs. Our mesoporous silica nanoparticle (MSN)-based nanozyme significantly enhanced the osteogenic marker gene expression and mineral deposition by the SSCs. Seahorse assay revealed a higher level of oxidative phosphorylation for the nanozyme group. In a CSBD model in rat femur, we found there was more bone regeneration in the MSN-based nanozyme group based on the μCT analysis. This innovative approach opens a new avenue for accelerating bone tissue regeneration via regulating the metabolic pathways of SSCs with mitochondrial-targeting nanozymes.
Funding Source: CUHK's Vice-Chancellor Early Career Professorship Scheme and the Shun Hing Institute of Advanced Engineering, CUHK (#BME-p2-24).
