Review examines immune dysfunction and emerging treatment targets in diabetic wounds

A review by Yi Ru and colleagues examines how immune cell populations change throughout diabetic wound healing and how disrupted responses may prevent resolution of inflammation. The authors consider monocytes, macrophages, neutrophils, mast cells, dendritic cells, and lymphocytes across inflammatory, proliferative, and remodeling stages. The supplied account does not report review methods or the number of included studies.

The review describes persistent pro-inflammatory macrophage states, dysregulated neutrophil extracellular traps, and excessive mast cell activation as potential contributors to tissue injury. Impaired clearance of apoptotic cells by dendritic cells may further sustain inflammation, with reduced SLC7A11 transporter activity implicated in this process. Reduced regulatory T-cell number and function and diminished activation of dendritic epidermal T cells may also impair repair. The authors acknowledge debate over the M1/M2 macrophage classification model.

Potential therapeutic approaches include topical anti-cytokine biologics, macrophage-modulating drugs, mesenchymal stem cells and their extracellular vesicles, and biomaterials delivering immune-modifying agents. The review emphasizes that effects may depend on the wound’s healing stage. Although the report mentions randomized trials of macrophage-regulating drugs, it provides no trial identifiers, sample sizes, effect estimates, or safety findings. These proposals therefore identify research directions rather than establish a basis for changing clinical management.