糖尿病皮肤伤口迁延难愈，治疗手段有限。研究表明，内皮祖细胞外泌体(EPC-Exos)可促进血管新生和内皮修复。我们前期工作发现：(1)EPC-Exos可加速糖尿病小鼠皮肤伤口愈合，降低糖尿病小鼠血清中氧化应激、炎症因子水平；(2)miRNA-221-3p在EPC-Exos中高表达，其靶基因可能调控AGE-RAGE信号通路介导的细胞损伤及血管功能障碍等。由此推测miRNA-221-3p在EPC-Exos促进糖尿病皮肤伤口愈合中发挥重要作用。本项目拟通过人标本、动物和细胞实验阐明：(1)miRNA-221-3p在糖尿病伴皮肤伤口患者中的表达变化；(2)miRNA-221-3p对糖尿病小鼠血管新生和伤口修复的作用；(3)miRNA-221-3p对高糖培养的原代小鼠皮肤微血管内皮细胞的作用及机制。该研究有助于明确miRNA-221-3p在调节糖尿病皮肤伤口愈合中发挥的作用，为临床治疗提供新途径。

Diabetic skin wounds are difficult to heal and treatment is limited. Studies have shown that endothelial progenitor exosomes (EPC-Exos) can promote angiogenesis and endothelial repair. Our previous work found that: (1) EPC-Exos can accelerate skin wound healing in diabetic mice, reduce the levels of oxidative stress and inflammatory factors in serum of diabetic mice; (2) MiRNA-221-3p is highly expressed in EPC-Exos, and its target gene may regulate AGE-RAGE signaling pathway-mediated cell damage, vascular dysfunction and so on. It is speculated that miRNA-221-3p may plays an important role in EPC-Exos promoting diabetic skin wounds healing. This project is intended to demonstrate through human specimens, animal and cell experiments: (1) Expression changes of miRNA-221-3p in patients with diabetes and skin wounds; (2) The effect of miRNA-221-3p on angiogenesis and wound repair in diabetic mice; (3) The effect and mechanism of miRNA-221-3p on primary mouse skin microvascular endothelial cells cultured in high glucose. This study helps to clarify the role of miRNA-221-3p in regulating wound healing in diabetic skin and provides a new approach to clinical treatment.