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Inhibiting the cytosolic function of CXXC5 accelerates diabetic wound healing by enhancing angiogenesis and skin repair. | LitMetric

AI Article Synopsis

  • Diabetic foot ulcers (DFUs) are serious complications of diabetes, and finding factors that influence their development is crucial for treatment.
  • The study identified CXXC-type zinc finger protein 5 (CXXC5) as a key negative regulator that suppresses the Wnt/β-catenin pathway, affecting wound healing in DFU patients and diabetic mice.
  • A small molecule called KY19334 was found to activate the Wnt/β-catenin pathway, accelerating wound healing and promoting blood vessel formation, suggesting a new therapeutic approach for treating DFUs.

Article Abstract

Diabetic wound healing, including diabetic foot ulcer (DFU), is a serious complication of diabetes. Considering the complexity of DFU development, the identification of a factor that mediates multiple pathogeneses is important for treatment. In this study, we found that CXXC-type zinc finger protein 5 (CXXC5), a negative regulator of the Wnt/β-catenin pathway, was overexpressed with suppression of the Wnt/β-catenin pathway and its target genes involved in wound healing and angiogenesis in the wound tissues of DFU patients and diabetes-induced model mice. KY19334, a small molecule that activates the Wnt/β-catenin pathway by inhibiting the CXXC5-Dvl interaction, accelerated wound healing in diabetic mice. The enhancement of diabetic wound healing could be achieved by restoring the suppressed Wnt/β-catenin signaling and subsequently inducing its target genes. Moreover, KY19334 induced angiogenesis in hindlimb ischemia model mice. Overall, these findings revealed that restorative activation of Wnt/β-catenin signaling by inhibiting the function of cytosolic CXXC5 could be a therapeutic approach for treating DFUs.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10474114PMC
http://dx.doi.org/10.1038/s12276-023-01064-3DOI Listing

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