Skin trauma, particularly chronic non-healing wounds, imposes significant economic and physical burdens on patients and their families. A defining feature of these wounds is persistent dysregulated inflammation, with macrophage efferocytosis playing a critical role. Efferocytosis—the programmed removal of apoptotic cells (ACs) by macrophages—is vital for resolving inflammation and facilitating tissue repair. In chronic wounds associated with systemic diseases such as diabetes, impaired macrophage efferocytosis hinders AC clearance, leading to prolonged inflammation and delayed healing. This review focuses on the molecular mechanisms regulating macrophage efferocytosis during inflammation and discusses clinical strategies to improve the healing of chronic wounds. This review outlines the key stages of wound healing, with particular emphasis on the molecular mechanisms that regulate macrophage efferocytosis during the inflammatory phase. Furthermore, it discusses clinical strategies, particularly peripheral blood mononuclear cell infusion, to restore efferocytosis and improve outcomes in diabetic foot ulcer treatment.
Gao et al. (2026) studied this question.