ArticleInternational journal of nanomedicine2025
Exosomes Derived From Human Mesenchymal Stem Cells Mitigate Follicular Interstitial Cell Ferroptosis via the miR-26a-5p/PTEN/GPX4 Axis in Rats with Chemotherapy-Induced Premature Ovarian Insufficiency.
Article in International journal of nanomedicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Current Status of Animal Models for Premature Ovarian Insufficiency: Similarities to Clinical Manifestations and Therapeutic Applications.Tissue engineering and regenerative medicine · 2026Review
- Lysine-specific demethylase 3A (KDM3A) protects against ovarian dysfunction in premature ovarian insufficiency by transcriptional activation of ATP-binding cassette sub-family A member 7 (ABCA7)-mediated mitochondrial homeostasis.Molecular biomedicine · 2026Article
- The Potentials of Stem Cell-Derived Exosomal MicroRNAs in Ferroptosis Modulation: Molecular Insights into Hepatoprotection, Neuroprotection, Cardioprotection, Renoprotection and Pulmonoprotection.Stem cell reviews and reports · 2026Review
- Umbilical cord mesenchymal stem cells and their extracellular vesicles attenuate cryopreservation-induced ovarian injury via the suppression of ferroptosis in an in vitro culture system.Materials today. Bio · 2026Article
- Advances in ferroptosis research in ovarian cancer: molecular mechanisms and therapeutic perspectives.American journal of cancer research · 2026Review
- Roles of exosomes in microenvironment-related premature ovarian insufficiency: mechanisms and therapeutic intervention.Reproductive biology and endocrinology : RB&E · 2025Review
- Bone marrow mesenchymal stem cells-derived exosomes protect against β-cell destruction models and kidney injury by suppressing ferroptosis.Scientific reports · 2025Article
- hUCMSCs restore ovarian function via angiopoietin 1/2 rebalance in POI rats.Journal of ovarian research · 2025Article
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11 authors.
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Abstract
Background: Premature ovarian insufficiency (POI) is a persistent condition in young women characterized by early follicular development disorders and reduced fertility. Research has found that exosomes derived from human umbilical mesenchymal stem cells (hUCMSC-Exo) have significant tissue repair effects. This study aims to investigate the therapeutic effect and potential molecular mechanism of hUCMSC-Exo on POI. Methods: In vivo experiments were conducted by intraperitoneally injecting the chemotherapy drug cyclophosphamide (CTX) to establish a 14-day POI rat model. Serum hormone levels were measured using an enzyme-linked immunosorbent assay, and changes in ovarian tissue structure were analyzed using hematoxylin-eosin (HE) staining. Perls staining and transmission electron microscopy were used to assess changes in ovarian ferroptosis. In vitro experiments involved exposing theca interna cells (TICs) treated with CTX to normal and miR-26a-5p inhibitor-treated hUCMSC-Exo. The expression changes of PTEN, Nrf2, and GPX4, which are associated with ferroptosis, were analyzed using immunofluorescence, Western blot, and quantitative reverse-transcription polymerase chain reaction. Results: hUCMSC-Exo intervention can significantly repair the ovarian tissue structure and functional abnormalities in the model rats, especially ferroptosis. Further bioinformatics analysis revealed that the inhibition of the PTEN/GPX4 pathway-mediated ferroptosis in TICs might be the main mechanism through which exosomes exert their regulatory/therapeutic effects. In vitro experiments, where exosome miR-26a-5p was inhibited, further confirmed that the delivery of miR-26a-5p is crucial for the regulatory effect of exosomes. Conclusion: In conclusion, our results suggest that hUCMSC-Exos alleviates POI-related dysfunction of ovarian structure and function. The mechanism could be related to the transfers of miR-26a-5p and suppression of PTEN/GPX4 axis signaling-mediated autophagy of TICs. It provides a new perspective for developing treatment methods for patients with metabolic abnormalities related to POI.
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