Editorial
Copyright ©The Author(s) 2025. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Diabetes. Jun 15, 2025; 16(6): 105615
Published online Jun 15, 2025. doi: 10.4239/wjd.v16.i6.105615
Epigenetics and diabetic wound healing: Wilms tumor 1-associated protein as a therapeutic target
Ashraf Al Madhoun
Ashraf Al Madhoun, Department of Genetics and Bioinformatics, Dasman Diabetes Institute, Dasman 15400, Kuwait
Author contributions: Al Madhoun A designed the overall concept, reviewed literature, wrote, and edited the manuscript.
Supported by the Kuwait Foundation for the Advancement of Sciences and Dasman Diabetes Institute, No. RACB-2021-007.
Conflict-of-interest statement: The author reports no relevant conflicts of interest for this article.
Open Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Ashraf Al Madhoun, PhD, Department of Genetics and Bioinformatics, Dasman Diabetes Institute, Jassim AlBahar Street, Dasman 15400, Kuwait. ashraf.madhoun@dasmaninstitute.org
Received: January 30, 2025
Revised: April 3, 2025
Accepted: May 12, 2025
Published online: June 15, 2025
Processing time: 134 Days and 20.3 Hours
Core Tip

Core Tip: Xiao et al identified the Wilms tumor 1-associated protein (WTAP)-DNA methyltransferase 1 (DNMT1) axis as a pivotal regulator of diabetic foot ulcer healing. Using human umbilical vein endothelial cells and a diabetic mouse model, those researchers demonstrated that WTAP knockdown restored endothelial cell function and enhanced angiogenesis and collagen deposition. Importantly, siRNA-mediated WTAP depletion markedly improved wound closure in the diabetic mice. Furthermore, DNMT1 reversed the beneficial effects of WTAP knockdown, confirming that it is a key downstream effector of WTAP.