ArticleStem cell research & therapy2025
MSC-derived exosomes improve endometrial fibrosis via the lncRNA IGF2R/ miR-143-5p/AQP8 axis.
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 3 papers.
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Who cites it
3 citing papers in PubMed.
- Endometrial Repair and Regenerative Medicine: From Broad-Spectrum Regeneration to Precision Intervention.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- Immunomodulatory and antimicrobial actions of extracellular vesicles in vaginal infections: implications for female infertility.Molecular biology reports · 2026Review
- Integrative bioengineering strategies for endometrial regeneration: From biomaterials and stem cells to organoids and organ-on-a-chip technologies.Theranostics · 2026Review
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9 authors.
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Abstract
backgroundEndometrial injury (EI) is frequently associated with intrauterine adhesions, endometrial thinning, amenorrhea, and infertility. In recent years, stem cells and their exosomes have been shown to have significant tissue repair efficacy. However, the role and probable mechanism of human umbilical cord mesenchymal stem cells (hUMSC-Exo) in endometrial healing remains unclear.
methodsTo build an EI model, in vivo investigations were carried out utilizing C57BL/6 mechanical manipulation. Hematoxylin-eosin staining and Masson Trichrome Staining were employed to examine morphological changes in the mouse uterus. TGF-β1 treatment was employed in an in vitro experiment to create an injury model for human endometrial stromal cells (hESCs). The expression of fibrosis-related molecules in uterine tissue and hESCs was investigated using Western blot and immunofluorescence labeling.
resultsIn animal experiments, after intervention with hUMSC-Exo, the fibrotic damage and expression of receptive molecules in the uterine tissue of EI mice were significantly repaired. Bioinformatics analysis predicts the high expression of lncRNA IGF2R in hUMSC-Exo and its relationship with fibrosis-related molecule aquaporin 8 (AQP8). In cell experiments, knocking down lncRNA IGF-2R in hUMSC-Exo or directly knocking down AQP8 in hESCs resulted in a significant increase in fibrosis-related molecule expression of hESCs.
conclusionsIn conclusion, our findings imply that hUMSC-Exo can prevent fibrosis via the AQP8/miR-143-5p/lncRNA IGF2R axis, hence reducing mechanically caused EI. Our findings offer fresh approaches and plans for using hUMSC-Exo to treat EI.
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