Objective To explore the effects of keratin 17 (Krt17) knockout on wound healing in diabetic mice. Methods To establish the diabetic model, a 60% high fat diet was provided and streptozotocin was administered intraperitoneally at 40 mg/ kg once per day for 5 consecutive days in wild type (WT) and Krt17 knockout (Krt17^{-/ -} ) mice at 6 weeks of age. The mice were anesthetized with isoflurane, the back was shaved, and a 6 mm circular skin lesion was made in vivo at 1 week after successful modeling. Western blot and immunofluorescence staining were used to assess the expression and localization of KRT17, and histopathology of wound healing was analyzed on day 8. Images were taken at 0, 2, 4, 6, and 8 days after wounding, and the wound healing rate was calculated. Results KRT17 was mainly expressed in mouse hair follicles under physiological conditions. When skin was injured, KRT17 expression in keratinocytes in the proximal wound was increased significantly. However, KRT17 expression in wounds of diabetic mice was significantly downregulated compared with that of control mice. The wound healing rate of Krt17^{-/ -} mice was significantly reduced and the local inflammatory reaction was more persistent compared with WT mice. Conclusions Krt17 knockout aggravates wound healing in diabetic mice. Krt17 may be an important modifier gene of diabetic wound healing.