Crosstalk between oxidative stress and inflammatory pathways: Natural therapeutic approaches for diabetic wound healing

Figure 2 Interactions between oxidative stress and inflammation in diabetic wounds. Hyperglycemia-induced oxidative stress and inflammation synergistically disrupt multiple stages of the wound healing process, including immune cell recruitment, angiogenesis, fibroblast activation, and extracellular matrix remodeling. These processes impair re-epithelialization and prolong chronic wound states. The interplay between M1/M2 macrophage polarization, ischemia, biofilm formation, and mesenchymal stem cell dysfunction further reinforces a self-perpetuating cycle of delayed tissue repair within the diabetic microenvironment. HIF: Hypoxia-inducible factor; HMOX-1: Heme oxygenase 1; IGF: Insulin-like growth factor; KGF: Keratinocyte growth factor; MMP: Matrix metalloproteinase; ROS: Reactive oxygen species; TIMP: Tissue inhibitor of metalloproteinases; VEGF: Vascular endothelial growth factor. Created in BioRender.