ArticleMolecular genetics and genomics : MGG2025
Placental mesenchymal stem cell-derived exosomes treat endometrial injury in a rat model of intrauterine adhesions.
Article in Molecular genetics and genomics : MGG, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Stem cell therapy for intrauterine adhesions: a systematic review and meta-analysis of clinical outcomes.BMC pregnancy and childbirth · 2025Pooled it
- Endometrial Repair and Regenerative Medicine: From Broad-Spectrum Regeneration to Precision Intervention.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- Unveiling the Pathological Landscape of Intrauterine Adhesion: Mechanistic Insights and Exosome-Biomaterial Therapeutic Innovations.International journal of nanomedicine · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intrauterine adhesion (IUA) refer to persistent inflammation and fibrosis due to damaged or infected endometrium and eventually lead to dysfunction. This study aimed to explore the therapeutic effects of exosomes (Exos) derived from placental mesenchymal stem cells (PMSCs) on endometrial repair in a rat model of IUA and to elucidate the underlying molecular mechanisms. PMSCs were characterized using flow cytometry and differentiation assays (osteogenic, adipogenic, and chondrogenic). Exos were isolated via ultracentrifugation and validated through transmission electron microscopy, nanoparticle tracking analysis and Western blot. An IUA model was established via electrocoagulation, and endometrial repair was assessed using hematoxylin-eosin (HE) and Masson staining. RNA sequencing, differential expression analysis and protein-protein interaction (PPI) network construction were employed to investigate the molecular mechanisms of PMSC Exos mediated repair. The role of miR-143 in targeting MyD88 and modulating the NF-κB signaling pathway was confirmed using Dual-Luciferase Reporter Assay and qRT-PCR. PMSC Exos significantly improved endometrial thickness, increased glandular number and reduced fibrosis in the IUA model. RNA sequencing and differential expression analysis screened 3980 differentially expressed genes (DEGs) common to the IUA vs normal groups and Exo vs IUA groups. Enrichment analysis revealed significant involvement of immune system processes, natural killer cell-mediated cytotoxicity and NF-κB signaling. PMSC Exos delivered miR-143, which targeted MyD88, thereby regulating the NF-κB pathway. PMSC Exos effectively repaired endometrial damage in the IUA model by modulating the NF-κB signaling pathway through miR-143 delivery. These findings suggest that PMSC Exos hold promise as a novel therapeutic strategy for IUA, offering insights into the molecular mechanisms underlying endometrial repair.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.