Role Of Dapk1 In Diabetic Oral Mucosal Chronic Wound Healing

This study aims to investigate the role of DAPK1 in chronic wound healing of diabetic oral mucosa and explore its underlying mechanisms, offering potential therapeutic targets for accelerating wound recovery in diabetic patients. 12-16 week-old WT/KO male mice were used, and ethical approval was obtained. Type I and Type II diabetes models were established using STZ induction, and a 1.5 mm diameter wound was created on the palatal mucosa of the mice using a circular punch. The experimental methods to be employed include gross observation, Masson staining, HE staining, Ki67 immunofluorescence staining, Western blotting, RT-qPCR, CCK-8 assay, scratch assay, plasmid transfection, siRNA knockdown, and high-throughput sequencing. DAPK1 global knockout diabetic mice showed a significantly faster wound healing rate compared to normal diabetic mice. Knockdown of DAPK1 promoted proliferation and migration of human oral keratinocytes under high-glucose conditions. The use of the DAPK1 inhibitor HS38, which inhibits its kinase activity, further demonstrated that the role of DAPK1 is dependent on its kinase activity. This study reveals the crucial role of DAPK1 in chronic wound healing of diabetic oral mucosa. Knockdown of DAPK1 or inhibition with the DAPK1 inhibitor accelerates wound healing, promotes proliferation and migration of keratinocytes, and this effect is dependent on the kinase activity of DAPK1, thereby enhancing re-epithelialization and accelerating the wound healing process in diabetic oral mucosa.