Macrophages regulate healing-associated fibroblasts in diabetic wounds. Diabetic wounds have impaired healing due to altered inflammation, angiogenesis, and fibrosis. Both macrophages and fibroblasts show phenotypic changes in diabetic wounds. A fibroblast subpopulation expressing high levels of MMP1, MMP3, MMP11, and CHI3L1 is associated with successful diabetic wound healing. However, the role of macrophages in regulating these fibroblasts is unclear. In a mouse model, diabetic wounds showed altered spatiotemporal changes in IL1β, IL6, IL10, and VEGF-A in macrophages, and reduced expression of MMP1, MMP3, MMP11, CHI3L1, and VEGF-A in fibroblasts. Co-culture with diabetic macrophages reduced fibroblast expression of these factors, while co-culture with non-diabetic macrophages or diabetic macrophages supplemented with IL6 increased their expression. IL6 treatment improved wound healing and angiogenesis in diabetic mice. Macrophages may induce activation of healing-associated fibroblasts, while defective macrophages in diabetes may be corrected with IL6 treatment as a promising therapy for diabetic foot disease. Macrophages play a critical role in wound healing by regulating fibroblast activation. In diabetes, macrophages are dysfunctional, impairing wound healing. IL6 treatment can correct this dysfunction, improving fibroblast activation and wound healing. This study highlights the importance of macrophage function in diabetic wound healing and suggests IL6 as a potential therapeutic strategy.Macrophages regulate healing-associated fibroblasts in diabetic wounds. Diabetic wounds have impaired healing due to altered inflammation, angiogenesis, and fibrosis. Both macrophages and fibroblasts show phenotypic changes in diabetic wounds. A fibroblast subpopulation expressing high levels of MMP1, MMP3, MMP11, and CHI3L1 is associated with successful diabetic wound healing. However, the role of macrophages in regulating these fibroblasts is unclear. In a mouse model, diabetic wounds showed altered spatiotemporal changes in IL1β, IL6, IL10, and VEGF-A in macrophages, and reduced expression of MMP1, MMP3, MMP11, CHI3L1, and VEGF-A in fibroblasts. Co-culture with diabetic macrophages reduced fibroblast expression of these factors, while co-culture with non-diabetic macrophages or diabetic macrophages supplemented with IL6 increased their expression. IL6 treatment improved wound healing and angiogenesis in diabetic mice. Macrophages may induce activation of healing-associated fibroblasts, while defective macrophages in diabetes may be corrected with IL6 treatment as a promising therapy for diabetic foot disease. Macrophages play a critical role in wound healing by regulating fibroblast activation. In diabetes, macrophages are dysfunctional, impairing wound healing. IL6 treatment can correct this dysfunction, improving fibroblast activation and wound healing. This study highlights the importance of macrophage function in diabetic wound healing and suggests IL6 as a potential therapeutic strategy.