适度的炎症反应对创面愈合至关重要。糖尿病溃疡创面难愈机制复杂，是创面治疗的难题，主要表现为炎症期延长、伴随表皮再生缺陷，寻找协同调控炎症反应与表皮再生的分子重要而紧迫。miR-31与炎症相关，参与多种皮肤疾病的病理过程，但未见与糖尿病溃疡创面难愈的报道。我们前期工作发现：糖尿病溃疡皮肤糖基化终末产物(AGEs)蓄积引发炎症紊乱导致伤口难愈；继而发现miR-31在糖尿病溃疡伤口皮肤表达异常，且参与炎症反应信号通路STAT3的调控，miR-31与表皮再生标志MMP-1正相关。由此提出科学假设：miR-31介导AGEs-STAT3-MMP1轴激活表皮细胞促进糖尿病溃疡伤口愈合。本项目拟从动物-组织-细胞-分子四个层次深入探索miR-31在糖尿病溃疡中的表达模式及其在糖尿病溃疡伤口愈合中的作用，进而系统阐明miR-31协同调控炎症反应和表皮再生的具体机制，为临床糖尿病溃疡伤口难愈防治提供科学依据。

Appropriate inflammatory response is critical for wound healing. Wound healing of diabetic ulcer is always a difficult problem in wound treatment and it is characterized by prolonged inflammatory period and defects in epidermal regeneration. It is important and urgent to find molecules that can coordinate the regulation of inflammatory response and epidermal regeneration. MiR-31 is closely related to inflammation, and it is involved in the pathophysiological process of a variety of skin diseases. So far, there have been no report of miR-31 for wound healing in diabetic ulcer. Our previous work showed that glycosylation end products (AGEs) accumulate around diabetes ulcer wound and promote excessive inflammation, which leads to slow wound healing; Subsequently, miR-31 was found to be abnormally expressed in the skin of diabetic ulcer wound and to be involved in the regulation of the inflammatory response signaling pathway STAT3. MiR-31 was positively correlated with the epidermal regeneration marker MMP-1. Based on these preliminary findings, we raised the hypothesis that miR-31 promotes wound healing by regulating AGEs-STAT3-MMP1 signal axis in diabetic ulcer. This project aims to explore the role of miR-31 in diabetic ulcers wound healing and update the understanding on the molecular pathology of diabetic ulcers wound healing. This research is highly significant to provide scientific evidences for the prevention, diagnosis and treatment of diabetic ulcers wound.