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Premature ovarian insufficient (POI) is one of the important causes of infertility in woman of reproductive age. At present, the clinical treatment of POI is limited and the therapeutic effect is not ideal. Extracellular vesicles derived from stem cells have attracted the attention of many researchers at home and abroad as a new cell-free therapy. Many animal experiment study shows that a variety of extracellular vesicles from stem cells carry microRNAs, lncRNAs, lipids, proteins, and other bioactive substances, improve ovarian function, affect granulosa cell proliferation and apoptosis, promote ovarian angiogenesis, and reduce oxidative stress response, thus playing a therapeutic role on POI. This article will review the mechanisms of extracellular vesicles in treatment of POI, and provide evidence for the application of extracellular vesicles in clinical treatment of POI.
, correspAuthors=Xiao-Feng Sun, authorNote=null, correspAuthorsNote=
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早发性卵巢功能不全(POI)是育龄期女性不孕的重要原因之一,目前临床治疗方法有限,治疗效果不理想。近年来,干细胞来源的细胞外囊泡作为一种新型的无细胞治疗方式备受关注。多项动物实验研究显示,各种干细胞来源的细胞外囊泡携带微小RNA、长链非编码RNA、脂质、蛋白质等多种生物活性物质,可改善卵巢功能、影响颗粒细胞增殖和凋亡、促进卵巢血管生成及减轻氧化应激反应,从而对POI发挥治疗作用。本文对干细胞来源的细胞外囊泡治疗POI的相关机制研究进行综述,旨在为其早日应用于POI的临床治疗提供依据。
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Mechanism and effect of extracellular vesicles from different stem cells in treatment of POI
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| 干细胞类型 | EVs类型 | 机制及效果 | 参考文献 |
|---|
| 脂肪间充质干细胞 | 外泌体 | 改善卵巢功能 通过SMAD途径影响GCs增殖和凋亡 | [23] |
| 骨髓间充质干细胞 | 外泌体 | 改善卵巢功能 携带miR-144-5p及miR-644-5p影响GCs的增殖和凋亡 促进卵巢血管的生成 | [24-26] |
| 脐带间充质干细胞 | 外泌体、EVs、微囊泡 | 改善卵巢功能 提高生殖能力 通过Hippo途径影响GCs增殖和凋亡以及卵巢功能 通过传递miR-17-5p抑制SRIT7,减轻氧化应激反应 促进卵巢血管生成 提高生育能力,对后代无影响 | [21,27-31] |
| 人羊膜间充质干细胞 | 外泌体 | 恢复卵巢功能 影响GCs的增殖与凋亡 通过miR-320a调节SIRT4,减轻氧化应激反应 提高生育能力 | [32] |
| 羊水间充质干细胞 | EVs | 恢复卵巢功能 携带miRNA-21,部分靶向PTEN和PI3K/PTEN,促进卵泡再生,抑制凋亡 | [33] |
| 胚胎干细胞 | EVs | 恢复卵巢功能 通过PI3K/Akt通路影响GCs增殖与凋亡 | [34] |
), ArticleFig(id=1199700883878543499, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1199688707377824285, language=CN, label=表1, caption=
不同干细胞来源的EVs治疗早发性卵巢功能不全的机制及效果
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| 干细胞类型 | EVs类型 | 机制及效果 | 参考文献 |
|---|
| 脂肪间充质干细胞 | 外泌体 | 改善卵巢功能 通过SMAD途径影响GCs增殖和凋亡 | [23] |
| 骨髓间充质干细胞 | 外泌体 | 改善卵巢功能 携带miR-144-5p及miR-644-5p影响GCs的增殖和凋亡 促进卵巢血管的生成 | [24-26] |
| 脐带间充质干细胞 | 外泌体、EVs、微囊泡 | 改善卵巢功能 提高生殖能力 通过Hippo途径影响GCs增殖和凋亡以及卵巢功能 通过传递miR-17-5p抑制SRIT7,减轻氧化应激反应 促进卵巢血管生成 提高生育能力,对后代无影响 | [21,27-31] |
| 人羊膜间充质干细胞 | 外泌体 | 恢复卵巢功能 影响GCs的增殖与凋亡 通过miR-320a调节SIRT4,减轻氧化应激反应 提高生育能力 | [32] |
| 羊水间充质干细胞 | EVs | 恢复卵巢功能 携带miRNA-21,部分靶向PTEN和PI3K/PTEN,促进卵泡再生,抑制凋亡 | [33] |
| 胚胎干细胞 | EVs | 恢复卵巢功能 通过PI3K/Akt通路影响GCs增殖与凋亡 | [34] |
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