ArticleJournal of assisted reproduction and genetics2026
Unraveling the VEGF-ETS1 axis: a transcriptomic and single-cell analysis of angiogenesis in endometriosis.
Article in Journal of assisted reproduction and genetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Endothelial cell heterogeneity drives angiogenesis in endometriosis: mechanisms and emerging organoid-based models.Apoptosis : an international journal on programmed cell death · 2026Review
- Multi-Target Modulation of Interconnected Pathogenetic Pathways by Natural Bioactive Compounds in Endometriosis.Antioxidants (Basel, Switzerland) · 2026Review
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Authors and funding
9 authors.
Funding
Abstract
purposeEndometriosis (EM) is a chronic inflammatory gynecological disorder characterized by ectopic endometrial-like lesions, where aberrant angiogenesis is a hallmark driving lesion establishment and progression. However, the transcriptional mechanisms underlying pathological vascular remodeling in EM remain unclear.
methodsIn this study, we identified E26 transformation-specific 1 (ETS1) as a key transcriptional regulator in EM pathogenesis through integrative analysis of bulk and single-cell transcriptomic datasets.
resultsAcross three independent transcriptome datasets and two validation cohorts, ETS1 expression was consistently elevated in endometriosis lesions, particularly in ovarian endometrioma. Single-cell RNA sequencing further revealed that ETS1 was predominantly expressed in endothelial cells and dynamically upregulated along the endothelial differentiation trajectory. Functional enrichment and pseudotime analyses indicated that ETS1 + endothelial cells exhibited enhanced angiogenic activity and vascular remodeling potential. Mechanistically, ETS1 amplified VEGF signaling by upregulating VEGFR1 and VEGFR2, while macrophage-derived VEGFA acted as the principal upstream activator within the lesion microenvironment.
conclusionsCollectively, our findings delineate the VEGF-ETS1 axis as a central driver of pathological angiogenesis in endometriosis, positioning ETS1 as both a mechanistic hallmark and a promising therapeutic target for endometriosis.
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