Figure 1.

Scheme revealing different factors associated with dysfunctional keratinocytes in diabetic wound healing. Advanced glycation end products (AGEs), reactive oxygen species (ROS), and inflammatory cytokines may contribute to the impairment of keratinocyte migration and proliferation, chronic inflammation, chronic infection, and impaired angiogenesis in high glucose environments, leading to impaired diabetic wound healing due to prolonged inflammation and the impaired proliferation phase of wound healing.