ArticleStem cell research & therapy2025
Harnessing extracellular vesicles from adipose-derived stem cells for the treatment of 4-vinylcyclohexene diepoxide-induced premature ovarian insufficiency.
Article in Stem cell research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Mesenchymal stem cell-based therapeutic strategies for female infertility: current evidence and emerging targeting approaches.Biotechnology letters · 2026Review
- miR-379-5p promotes ovarian granulosa cell apoptosis in primary ovarian insufficiency by targeting KNDC1 and PEG10.Frontiers in genetics · 2026Article
- Recent advances in methods for establishing animal models of premature ovarian failure.Journal of ovarian research · 2025Review
- Mesenchymal stem cells and extracellular vesicles for knee osteoarthritis: clinical application, mechanism exploration and prospect.Stem cell research & therapy · 2025Review
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14 authors.
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Abstract
backgroundPremature ovarian insufficiency (POI) is a challenging condition with limited effective treatments. Adipose-derived stem cells (ADSCs) have demonstrated potential in tissue repair, and their extracellular vesicles (ADSC-EVs) show more safety in clinical translation. However, the role and mechanism of ADSC-EVs in the treatment of POI are not yet fully understood. This study aims to investigate the protective effects of ADSC-EVs on rat POI models induced by 4-vinylcyclohexene diepoxide (VCD) and to explore the potential therapeutic mechanisms.
methodsRat ADSCs and ADSC-EVs were isolated and characterized. The POI rat model was established via intraperitoneal injection of VCD for 15 consecutive days. ADSCs and ADSC-EVs were injected into the ovaries for treatment. Ovary function was assessed by monitoring estrous cycles, follicle counts, sexual hormone levels, and ovulation. Molecular mechanisms were investigated using TUNEL staining, immunohistochemistry, quantitative polymerase chain reaction, and western blotting. In vitro, primary rat granulosa cells were treated with VCD in the presence or absence of ADSC-EVs. Cell proliferative ability, hormone secretion, apoptosis rate, and relative molecular expression were measured. Whole-transcriptome sequencing and DIA proteomics of ADSC-EVs were performed to identify bioactive molecules.
resultsADSC-EVs protected granulosa cells from VCD-induced apoptosis, promoted cell proliferation, enhanced hormone secretion, and upregulated KITL expression. Treatment with ADSCs and ADSC-EVs in POI rats significantly improved estrous cycles, follicle counts, and serum levels of estradiol (E2), follicle-stimulating hormone (FSH), and anti-Müllerian hormone (AMH). These treatments activated the KITL/KIT/PI3K/AKT signaling pathway, downregulated pro-apoptotic genes (Bax, Caspase3), and upregulated anti-apoptosis genes (Bcl2). ADSC-EVs are highly enriched in mRNA of Kit and PI3K, and both transcriptomic and proteomics enrichment analysis predominantly focused on PI3K/AKT pathway.
conclusionsADSCs and ADSC-EVs effectively protect and restore ovarian function in VCD-induced POI rats. The mechanism involves inhibiting apoptosis in granulosa cells and activating the KITL/KIT/PI3K/AKT pathway in ovary. ADSC-EVs, with advantages in clinical translation, hold significant potential for POI treatment.
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