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糖尿病足潰瘍是糖尿病的典型并發(fā)癥，在糖尿病患者中發(fā)病率高達(dá)4％。其發(fā)病誘因復(fù)雜多樣，通常難以愈合且復(fù)發(fā)率高。已有研究發(fā)現(xiàn)，從某些細(xì)胞類(lèi)型中分離得到的外泌體能夠促進(jìn)糖尿病傷口的愈合。然而，II型糖尿病（type 2 diabetes mellitus，T2DM）患者的循環(huán)外泌體對(duì)傷口愈合的影響仍不清楚。

近日，來(lái)自華中科技大學(xué)同濟(jì)醫(yī)學(xué)院附屬協(xié)和醫(yī)院的劉國(guó)輝、米博斌等合作研究了糖尿病患者外泌體特定miRNA在糖尿病足治療中的潛在作用，相關(guān)研究結(jié)果發(fā)表在Small雜志上。該研究鑒定了II型糖尿病患者的循環(huán)外泌體miRNA，觀察到外泌體miR-20b-5p顯著上調(diào)，且該miRNA能夠通過(guò)調(diào)節(jié)Wnt9b/β-catenin信號(hào)傳導(dǎo)抑制人臍靜脈內(nèi)皮細(xì)胞的血管生成，將miR-20b-5p或糖尿病外泌體處理傷口部位則會(huì)減緩傷口愈合和血管生成。在糖尿病小鼠模型中，研究人員發(fā)現(xiàn)敲除miR-20b-5p可以顯著增強(qiáng)傷口愈合并促進(jìn)傷口血管生成，提示miR-20b-5p在T2DM患者的外泌體中高度富集并且可以轉(zhuǎn)移到血管內(nèi)皮細(xì)胞中，靶向Wnt9b信號(hào)傳導(dǎo)來(lái)調(diào)節(jié)細(xì)胞功能和血管生成，為改善糖尿病相關(guān)的傷口愈合不良提供新策略。

Circulating Exosomal miR-20b-5p Inhibition Restores Wnt9b Signaling and Reverses Diabetes-Associated Impaired Wound Healing.

At present, developing therapeutic strategies to improve wound healing in individuals with diabetes remains challenging. Exosomes represent a promising nanomaterial from which microRNAs (miRNAs) can be isolated. These miRNAs have the potential to exert therapeutic effects, and thus, determining the potential therapeutic contributions of specific miRNAs circulating in exosomes is of great importance. In the present study, circulating exosomal miRNAs are identified in diabetic patients and assessed for their roles in the context of diabetic wound healing. A significant upregulation of miR-20b-5p is observed in exosomes isolated from patients with type 2 diabetes mellitus (T2DM), and this miRNA is able to suppress human umbilical vein endothelial cell angiogenesis via regulation of Wnt9b/β-catenin signaling. It is found that the application of either miR-20b-5p or diabetic exosomes to wound sites is sufficient to slow wound healing and angiogenesis. In diabetic mice, it is found that knocking out miR-20b-5p significantly enhances wound healing and promotes wound angiogenesis. Together, these findings thus provide strong evidence that miR-20b-5p is highly enriched in exosomes from patients with T2DM and can be transferred to cells of the vascular endothelium, where it targets Wnt9b signaling to negatively regulate cell functionality and angiogenesis.