| First Author | Kim E | Year | 2023 |
| Journal | Exp Mol Med | Volume | 55 |
| Issue | 8 | Pages | 1770-1782 |
| PubMed ID | 37524876 | Mgi Jnum | J:343165 |
| Mgi Id | MGI:7527068 | Doi | 10.1038/s12276-023-01064-3 |
| Citation | Kim E, et al. (2023) Inhibiting the cytosolic function of CXXC5 accelerates diabetic wound healing by enhancing angiogenesis and skin repair. Exp Mol Med 55(8):1770-1782 |
| abstractText | 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/beta-catenin pathway, was overexpressed with suppression of the Wnt/beta-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/beta-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/beta-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/beta-catenin signaling by inhibiting the function of cytosolic CXXC5 could be a therapeutic approach for treating DFUs. |
