Research Progress on the Mechanisms of Exosome-Based Therapy for Premature Ovarian Failure
卵巢早衰(Premature ovarian failure, POF)是一种近年发病率不断升高的妇科内分泌疾病,常导致不孕并伴随多种类似于更年期症状。目前POF病因暂不明确,治疗效果尚未达到预期,因此需要探索POF的新型治疗方式,改善卵巢功能,促进女性患者生育能力的恢复。外泌体广泛存在于血液、唾液、脑脊液等人体液体成分中,由脂质、蛋白质、RNA、DNA和其他与细胞来源相关的物质组成,介导细胞间的信息交流。大量研究表明,外泌体对于治疗卵巢疾病至关重要,可能作为重要靶点参与卵巢疾病的治疗过程,通过促进颗粒细胞功能恢复、促进卵巢再生、减少炎症、增强血管生成以及减轻氧化应激等各个方面对POF的治疗起到一定作用。现就当前外泌体对卵巢早衰的治疗作如下综述,以期为外泌体相关理论在POF的后续研究和治疗中提供参考。 Premature ovarian failure (POF) is a gynecological endocrine disease with an increasing incidence in recent years. It often leads to infertility and is accompanied by various symptoms similar to those of menopause. Currently, the etiology of POF remains unclear, and the treatment effect has not yet met expectations. Therefore, it is necessary to explore new treatment methods for POF to improve ovarian function and promote the recovery of fertility in female patients. Exosomes are widely present in human body fluid components such as blood, saliva, and cerebrospinal fluid. They are composed of lipids, proteins, RNA, DNA, and other substances related to cell origin, and mediate intercellular communication. A large number of studies have shown that exosomes are crucial for the treatment of ovarian diseases. They may participate in the treatment process of ovarian diseases as important targets and play a certain role in the treatment of POF in various aspects, such as enhancement of granulosa cell functional recovery, promotion of ovarian regeneration, reduction of inflammation, augmentation of angiogenesis, and alleviation of oxidative stress. This article reviews the current treatment of premature ovarian failure with exosomes, aiming to provide a reference for the subsequent research and treatment of POF using exosome-related theories.
Authors
- 杰 陈
Publication Details
- Journal
- Advances in Clinical Medicine
- Published
- 2025-01-01
- DOI
- https://doi.org/10.12677/acm.2025.1551520
- Primary Topic
- Extracellular vesicles in disease
- Type
- article
- Field-Weighted Citation Impact
- 0.00