Elabela inhibits TRAF1/NF-κB induced oxidative DNA damage to promote diabetic foot ulcer wound healing

• DOI: 10.1016/j.isci.2023.107601
• Publication Date: 2023-08-10T01:10:59Z
• Authors: Yinghui Hong; Jun Li; Yinsheng Zhong; Shujun Yang; Liying Pei; Zijie Huang; Xuxiang Chen; Hao Wu; Guanghui Zheng; Chaotao Zeng; Haidong Wu; Tong Wang
• Keywords: Diabetic foot ulcer

Diabetic foot ulcer (DFU) is a serious complication of diabetes. Elabela (ELA), ligand apelin receptor (APJ), was shown to promote angiogenesis and suppress inflammation. This study aimed illustrate the role ELA in DFU wound healing. A whole-skin defect model constructed using db/m db/db mice observe effects on The function endothelial cells cultured high glucose medium investigated. Administration peri-wound area accelerated closure reduced inflammatory infiltration. Indicators DNA damage, elevated reactive oxygen species (ROS) levels tail amounts, were downregulated by but compromised after TRAF1 overexpression. ELA-mediated inhibition NF-κB phosphorylation improved cell migration angiogenesis, which blocked APJ silencing. findings imply that suppresses TRAF1-mediated signal activation, reducing ROS-related oxidative damage improving protection function.