ArticleEuropean journal of histochemistry : EJH2025
Placental mesenchymal stem cell exosomes drive macrophage M2 polarization
Article in European journal of histochemistry : EJH, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
- Advancing Human Placental Modeling Through Stem-Cell-Derived Trophoblast Organoids and Reprogramming Innovations.Biomedicines · 2026Review
- Research Advances on Mesenchymal Stem Cell-Derived Exosomes in Anti-Graft-Versus-Host Disease Therapy: Mechanisms, Therapeutic Potential, and Future Prospects.International journal of molecular sciences · 2026Review
- A network pharmacology-based study on the mechanism of hirudin attenuates renal interstitial fibrosis through Nrf2 and NF-κB signalling pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The functional state of placental mesenchymal stem cells (PMSCs) plays a critical role in maintaining maternal-fetal interface homeostasis during the pathogenesis of preeclampsia (PE). Given the limitations associated with direct stem cell transplantation, this study aimed to investigate the therapeutic potential of PMSC-derived exosomes and their carried miR-146a-5p. Clinical sample analysis revealed a significant downregulation of miR-146a-5p in placental tissues from PE patients, accompanied by impaired proliferation, migration, and angiogenic dysfunction of PMSCs. In an in vitro model, exosome intervention effectively reversed hypoxia-induced trophoblast cell apoptosis and enhanced migratory capacity. Furthermore, it promoted macrophage polarization towards the anti-inflammatory M2 phenotype and markedly improved the inflammatory cytokine secretion profile. In a PE mouse model, exosome treatment reduced maternal blood pressure and proteinuria levels, alleviated fetal growth restriction, and up-regulated the expression of M2 macrophage markers in placental tissue. Mechanistically, miR-146a-5p targeted TRAF6 to suppress NF-κB pathway activation, an effect that could be reversed by specific inhibitors. This study is the first to demonstrate that PMSC-derived exosomes, via the miR-146a-5p/TRAF6 axis, concurrently ameliorate trophoblast dysfunction and correct macrophage polarization imbalance. The efficient intercellular delivery of miR-146a-5p by exosomes underscores their potential as a novel targeted therapeutic strategy for PE.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.