Abstract
In this editorial, we discuss the article by Wen et al published. Diabetic foot ulcers are prevalent and serious complications of diabetes, significantly impacting patients' quality of life and often leading to disability or death, thereby placing a heavy burden on society. Effective diabetic wound healing is hindered by an imbalance in macrophage polarization; many macrophages fail to transition from the pro-inflammatory M1 phenotype to the anti-inflammatory M2 phenotype, which is crucial for tissue remodelling and repair. The wound healing process is both dynamic and complex. Healthy M1 macrophages, which have strong phagocytic abilities, are vital during the inflammatory phase of diabetic wound healing. However, the failure to transition to M2 macrophages during the proliferative phase hinders wound healing. We anticipate the development of new therapies that can repair damaged M1 macrophages during the inflammatory phase and promote M2 macrophage polarization during the proliferative phase, thereby enhancing the overall healing process.