Wound healing disorder after severe burn trauma is a significant clinical challenge， and the primary pathological factor is insufficient neovascularization. Endothelial progenitor cells （EPCs） home to the injured site and participate in angiogenesis， playing a crucial role in reconstructing the blood supply and promoting tissue regeneration. The signaling axis composed of stromal cell-derived factor-1 （SDF-1） and its receptor C-X-C chemokine receptor type 4 （CXCR4） is the main system regulating the homing chemotaxis of EPCs. Microenvironmental changes such as ischemia， hypoxia， and inflammation in the local wound area after burn trauma induce the upregulation of SDF-1 expression， forming a concentration gradient to recruit EPCs from the circulatory system. Activation of the SDF-1/CXCR4 axis regulates downstream pathways such as phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) and mitogen-activated protein kinase (MAPK)， thereby modulating the migration， survival， proliferation， and differentiation of EPCs. Furthermore， this signaling axis forms a complex regulatory network with pathways including Wnt/β-catenin， tyrosine kinase (JAK)/transcriptional activator protein (STAT)， and hypoxia-inducible factor (HIF)， and coordinates the interaction between EPCs and various cell types， such as fibroblasts and immune cells， to jointly achieve wound repair. Therefore， this review elaborates on the molecular mechanisms of the SDF-1/CXCR4 signaling pathway in burn wound repair. It deeply explores the regulatory network of this pathway， related therapeutic strategies， challenges in clinical translation， and discusses future research directions in the field of burn and trauma medicine. This review aims to provide a theoretical basis and new perspectives for the development of SDF-1/CXCR4-targeted therapies to promote wound healing.