ArticleJournal of extracellular vesicles2026
Human Endometriotic Lesion-Derived Small Extracellular Vesicles Impair Macrophage Function in the Peritoneal Microenvironment.
Article in Journal of extracellular vesicles, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Phytochemicals Modulating Receptor Tyrosine Kinase Signaling Networks in Endometriosis.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Is Recurrent Endometriosis a Reprogrammed Disease? Molecular Persistence Beyond Surgical Clearance.Cells · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
Endometriosis (EM) is a chronic inflammatory disease that affects ∼10% of women during reproductive age. It is characterised by ectopic (ECT) growth of endometrial-like tissue mainly in the pelvic cavity. Small extracellular vesicles (sEVs) mediate cellular interactions, but their function remains poorly understood in the pathogenesis of EM. 3D endometrial epithelial organoids (EEOs) from ECT lesions and eutopic (EUT) endometrium from EM patients and controls were established to investigate sEVs. Multiplex bead-based flow cytometry revealed CD133/1 and EpCAM as dominant markers on EEO-sEVs, with ECT EEO-sEVs showing upregulation of CD44, CD29 and downregulation of EpCAM compared to EUT EEO-sEVs. Peritoneal fluid (PF)-sEVs displayed high and correlated CD133/1 and EpCAM expression, indicating a major contribution from endometrial epithelial (EE) cells, alongside sEVs of lymphocyte and endothelial origin. Functionally, both ECT EEO-sEVs and PF-sEVs from EM patients significantly suppressed macrophage phagocytosis, as assessed by pH-sensitive fluorescent bioparticles. The effect was reversed by CD47 blockade. The coexpression of CD47 with CD133/1 and EpCAM on PF-sEVs indicates the involvement of EE cell-derived sEVs in CD47/SIRP-α mediated suppression. This study provides the first thorough characterisation of EE-derived sEVs utilising EEO models in EM and demonstrates their potential immunomodulatory role in the peritoneal microenvironment via CD47/SIRP-α signalling.
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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.