The issue of delayed wound healing or nonhealing in diabetic patients presents a challenge for modern medicine. A number of attempts have been made to understand the mechanisms behind diabetic wound. In a hyperglycemic environment, increased intracellular reactive oxygen species (ROS) disturb the balance between oxidation and antioxidant, causing the wound environment to deteriorate. It has been established that the nuclear factor E2-related factor 2 (Nrf2) and nuclear factor-kappa B (NF-κB) pathways play an important role in regulating inflammation and oxidative stress. Several potential treatment strategies involving Nrf2 and/or NF-κB pathways have been explored in previous studies. Hence, we analyzed mechanisms and changes in Nrf2 and NF-κB pathways in response to oxidative stress and inflammation in diabetic environment. Additionally, we reviewed potential treatment strategies from the past five years for diabetic wound by Nrf2 and/or NF-κB pathways, including receptor agonists, vitamins, hormones, exosomes, drugs, plants, and biomaterials. It may be useful to develop drugs to promote diabetic wound healing.
Keywords: Diabetes; Oxidative stress; Tissue regeneration; Wound.
© 2023. The Author(s), under exclusive licence to Springer Nature B.V.