Asset Details
Do you wish to reserve the book?
Inhibiting the cytosolic funaction of CXXC5 accelerates diabetic wound healing by enhancing angiogenesis and skin repair
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Inhibiting the cytosolic funaction of CXXC5 accelerates diabetic wound healing by enhancing angiogenesis and skin repair
Do you wish to request the book?
Inhibiting the cytosolic funaction of CXXC5 accelerates diabetic wound healing by enhancing angiogenesis and skin repair
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Inhibiting the cytosolic funaction of CXXC5 accelerates diabetic wound healing by enhancing angiogenesis and skin repair
2023
Overview
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. KCI Citation Count: 15
Publisher
생화학분자생물학회
Subject
We currently cannot retrieve any items related to this title. Kindly check back at a later time.