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Metformin accelerates bone fracture healing by promoting type H vessel formation through inhibition of YAP1/TAZ expression. | LitMetric

AI Article Synopsis

  • Fractures are increasingly recognized as a public health issue, prompting research into the effects of metformin on healing in osteoporotic and normal fractures.
  • The study found that metformin accelerates fracture healing and promotes the formation of type H vessels, which are important for bone healing, by increasing HIF-1α levels and inhibiting YAP1/TAZ expression.
  • Overall, the findings indicate that metformin could be a promising treatment for enhancing fracture recovery by fostering type H vessel development through YAP1/TAZ inhibition.

Article Abstract

Due to increasing morbidity worldwide, fractures are becoming an emerging public health concern. This study aimed to investigate the effect of metformin on the healing of osteoporotic as well as normal fractures. Type H vessels have recently been identified as a bone-specific vascular subtype that supports osteogenesis. Here, we show that metformin accelerated fracture healing in both osteoporotic and normal mice. Moreover, metformin promoted angiogenesis in vitro under hypoxia as well as type H vessel formation throughout fracture healing. Mechanistically, metformin increased the expression of HIF-1α, an important positive regulator of type H vessel formation, by inhibiting the expression of YAP1/TAZ in calluses and hypoxia-cultured human microvascular endothelial cells (HMECs). The results of HIF-1α or YAP1/TAZ interference in hypoxia-cultured HMECs using siRNA further suggested that the enhancement of HIF-1α and its target genes by metformin is primarily through YAP1/TAZ inhibition. Finally, overexpression of YAP1/TAZ partially counteracted the effect of metformin in promoting type H vessel-induced angiogenesis-osteogenesis coupling during fracture repair. In summary, our findings suggest that metformin has the potential to be a therapeutic agent for fractures by promoting type H vessel formation through YAP1/TAZ inhibition.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10432554PMC
http://dx.doi.org/10.1038/s41413-023-00279-4DOI Listing

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