Evidence map›Paper›PMID 41543773›Full record

ArticleJournal of assisted reproduction and genetics2026

Unraveling the VEGF-ETS1 axis: a transcriptomic and single-cell analysis of angiogenesis in endometriosis.

Xiaoxuan Liu, Ran An, Ping Zhang, Qi Yang, Shuang Wang, Xue Jiao, Le Xu, Qianhui Ren, Guoyun Wang

Abstract read
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Review
  2. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Xiaoxuan LiuDepartment of Obstetrics and Gynecology, Shandong Provincial Hospital, Shandong University, Jinan, 250000, Shandong, China.
Ran AnThe Second Hospital of Shandong University, Jinan, Shandong, China.
Ping ZhangDepartment of Obstetrics and Gynecology, Shandong Provincial Hospital, Shandong University, Jinan, 250000, Shandong, China.
Qi YangSchool of Mathematics, Shandong University, Jinan, China.
Shuang WangDepartment of Obstetrics and Gynecology, Shandong Provincial Hospital, Shandong University, Jinan, 250000, Shandong, China.
Xue JiaoDepartment of Obstetrics and Gynecology, Shandong Provincial Hospital, Shandong University, Jinan, 250000, Shandong, China.
Le XuJiNan Key Laboratory of Diagnosis and Treatment of Major Gynaecological Disease, Jinan, 250000, Shandong Province, China.
Qianhui RenJiNan Key Laboratory of Diagnosis and Treatment of Major Gynaecological Disease, Jinan, 250000, Shandong Province, China.
Guoyun WangDepartment of Obstetrics and Gynecology, Shandong Provincial Hospital, Shandong University, Jinan, 250000, Shandong, China. wangguoy@sdu.edu.cn.ORCID http://orcid.org/0000-0003-4023-084X

Funding

General Project of Shandong Natural Science Foundation ZR2023MH177the Major Basic Research of Natural Science Foundation of Shandong ZR2021ZD34The National Key R&D Program of China 2022YFC2704000the National Natural Science Foundation of China 82071621the National Natural Science Foundation of China grant numbers 82371653the Special foundation for Taishan Scholars No. tstp20230657
6 · The paper itself

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.

Indexed as

AngiogenesisEndometriosisNeovascularization, PathologicProto-Oncogene Protein c-ets-1Vascular Endothelial Growth Factor AEndometriumEndothelial CellsFemaleHumansSignal TransductionSingle-Cell AnalysisSingle-Cell Gene Expression AnalysisTranscriptomeVascular Endothelial Growth Factor Receptor-1Vascular Endothelial Growth Factor Receptor-2ETS1 protein, humanProto-Oncogene Protein c-ets-1Vascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-1Vascular Endothelial Growth Factor Receptor-2VEGFA protein, humanAngiogenesisEndometriosisEndothelial cellsETS1Single-cell RNA sequencingTranscriptomicsVEGFVEGF-ETS1 axis

Identifiers

PMID41543773
PMCPMC12982733

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.