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中华损伤与修复杂志(电子版) ›› 2026, Vol. 21 ›› Issue (02) : 154 -159. doi: 10.3877/cma.j.issn.1673-9450.2026.02.013

综述

基质细胞衍生因子-1/C-X-C趋化因子受体4信号轴调控内皮祖细胞归巢促进创面愈合分子机制的研究进展
吴玉杰1, 周雨婷1, 马晓婷1, 余小平2,()   
  1. 1 730000 兰州,甘肃中医药大学
    2 730000 兰州,甘肃省人民医院烧伤科
  • 收稿日期:2025-12-26 出版日期:2026-04-01
  • 通信作者: 余小平
  • 基金资助:
    甘肃省卫生健康行业科技创新重大项目(GSWSQNPY2025-18); 兰州市科技计划项目(2022-ZD-45); 甘肃省烧伤与创面修复临床医学研究中心(21JR7RA674)

Research progress on the molecular mechanism of stromal cell-derived factor-1/C-X-C chemokine receptor type 4 regulating endothelial progenitor cell homing to promote wound healing

Yujie Wu1, Yuting Zhou1, Xiaoting Ma1, Xiaoping Yu2,()   

  1. 1 Gansu University of Chinese Medicine,Lanzhou 730000,China
    2 Department of Burn,Gansu Provincial Hospital,Lanzhou 730000,China
  • Received:2025-12-26 Published:2026-04-01
  • Corresponding author: Xiaoping Yu
引用本文:

吴玉杰, 周雨婷, 马晓婷, 余小平. 基质细胞衍生因子-1/C-X-C趋化因子受体4信号轴调控内皮祖细胞归巢促进创面愈合分子机制的研究进展[J/OL]. 中华损伤与修复杂志(电子版), 2026, 21(02): 154-159.

Yujie Wu, Yuting Zhou, Xiaoting Ma, Xiaoping Yu. Research progress on the molecular mechanism of stromal cell-derived factor-1/C-X-C chemokine receptor type 4 regulating endothelial progenitor cell homing to promote wound healing[J/OL]. Chinese Journal of Injury Repair and Wound Healing(Electronic Edition), 2026, 21(02): 154-159.

严重烧创伤后创面愈合障碍是临床上面临的一个棘手问题,其关键病理环节在于新生血管不足。内皮祖细胞(EPCs)归巢至损伤部位参与血管生成,对血管生成、促进组织再生具有重要作用。基质细胞衍生因子-1(SDF-1)及其受体C-X-C族趋化因子受体4(CXCR4)构成的信号轴是调节EPCs归巢趋化的主要系统。烧创伤后创面局部缺血、缺氧、炎症等微环境变化可诱导SDF-1表达上调,并形成浓度梯度,从而招募循环系统中的EPCs。SDF-1/CXCR4的激活可调控磷脂酰肌-3-激酶(PI3K)/蛋白激酶B(Akt)和丝裂原活化蛋白激酶(MAPK)等下游通路,进而调节EPCs的迁移、存活、增殖与分化。此外,该信号轴还与Wnt/β-连环蛋白(β-catenin)、酪氨酸激酶(JAK)/转录激活蛋白(STAT)和缺氧诱导因子(HIF)等通路形成复杂的调节网络,并协调EPCs与成纤维细胞、免疫细胞等多种细胞的相互作用,共同完成创面修复。因此,有必要对SDF-1/CXCR4信号通路在烧伤创面修复中分子机制及作用进行综述,深入探讨该通路的调节网络、治疗策略以及临床转化面临的诸多挑战,并对未来在烧创伤医学领域的研究方向进行展望,旨在为开发靶向SDF-1/CXCR4促创面愈合方法提供理论基础和新视角。

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.

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