FOXO1 Plays a Key Role in Wound Healing

The re-epithelialization, involving keratinocyte migration and proliferation, begins after damage. Keratinocyte mobilization is a critical aspect of wound re-epithelialization, but the mechanisms that control its precise regulation remain poorly understood. The transcription factor, Forkhead Box Protein O1 (FOXO1), has been recently found to be an important regulator of wound healing. FOXO1 is protecting keratinocytes from oxidative stress by regulating antioxidant genes in wound healing. The aim of this review is to investigate positive effect of FOXO1 in wound healing. Previous research has shown that the decrease in FOXO1 levels affects other genes involved in cell migration which. The researchers found that many of these genes were significantly less pronounced, especially the gene related to TGF-B1, which is a vital growth factor in wound healing. It has been suggested that FOXO1 stimulates TGF-B promoter activity resulting in the upregulation of TGF-B expression. Increased TGF-B stimulates expression of integrins and matrix metalloproteinases to improve wound healing through increased keratinocyte migration and decreased apoptosis. Oxidative stress increases in cells lacking FOXO1. Oxidation stress is harmful to wound healing. The wound repair environment is a stressful environment for the cell; it seems that the high-level FOXO1 settings protect the cell from oxidative stress. The results of this study showed that FOXO1 has an integral role in two key processes in wound healing: activation of TGF-B1 and protection of cells against oxidative degradation.

Keywords:

Wound Healing , Stress Oxidative , FOXO1 , TGF-B1