Endothelial cell heterogeneity drives angiogenesis in endometriosis: mechanisms and emerging organoid-based models

Jingjing Xu, Xu J, Tan Y, Yadan Tan, Ziteng Huang, Huang Z, Wang X, Xiran Wang, Song L, Lihong Song, Jinshan Xing, Xing J, Li R, Rong Li, Yi J
Apoptosis : an international journal on programmed cell death · 2026 · vol. 31(9) · doi:10.1007/s10495-026-02427-7 · PMID:42622720 · W7203826939
review OA: closed public-domain-us
View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by qwen3.7-flash, 2026-08-22 ⓘ

This review examines how endothelial cell heterogeneity drives angiogenesis in endometriosis and highlights biomaterial-supported organoid models as physiologically relevant tools for dissecting these mechanisms and developing targeted therapeutic strategies.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

Abstract

Endometriosis (EMs) is characterized by the establishment and persistence of ectopic lesions, a process fundamentally dependent on aberrant angiogenesis. Endothelial cells (ECs) play a central role in this process; however, accumulating evidence indicates that ECs are not a homogeneous population but comprise multiple subtypes with distinct molecular signatures and functional states, including quiescent, proliferative, hormone-responsive and inflammation-associated phenotypes. The initiation and maintenance of pathological angiogenesis in EMs are coordinately regulated by hormonal signaling, inflammatory responses and immune modulation, which collectively determine vascular remodeling and lesion sustainability. Despite significant advances, mechanistic insights into EMs-associated angiogenesis have been limited by the lack of physiologically relevant experimental models. Conventional two-dimensional culture systems fail to recapitulate the complex three-dimensional cellular interactions, whereas animal models are constrained by interspecies differences. Recent progress in stem cell biology, extracellular matrix (ECM) engineering and microfluidic technologies has enabled the development of organoid-based platforms that more faithfully reconstruct the EMs microenvironment. When integrated with functional biomaterials possessing tunable mechanical properties and bioactivity, these systems allow precise modulation of endothelial behaviors, including proliferation, migration and lumen formation, through controlled delivery of angiogenic cues. In this Review, we summarize recent advances in biomaterial-supported organoid systems for dissecting endothelial cell heterogeneity and its contribution to aberrant angiogenesis in EMs. We further discuss their emerging roles in mechanistic studies and the development of targeted therapeutic strategies.

My notes (saved in your browser only)

MeSH descriptors

Angiogenesis Angiogenesis Angiogenesis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endothelial Cells Endothelial Cells Endothelial Cells Endothelial Cells Endothelial Cells Neovascularization, Pathologic Neovascularization, Pathologic Neovascularization, Pathologic Neovascularization, Pathologic Organoids Organoids Organoids

Funding

funders
[{'doi': '10.13039/501100001809', 'name': 'National Natural Science Foundation of China', 'awards': ['82301845']}, {'doi': '10.13039/100012542', 'name': 'Sichuan Provincial Science and Technology Support Program', 'awards': ['2025ZNSFSC1665']}]

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (100)

SciLite annotations

organisms 1
rodents

Source provenance

crossref
last seen: 2026-08-21T06:36:46.985616+00:00
europepmc
last seen: 2026-08-23T09:30:01.253652+00:00
openalex
last seen: 2026-08-23T06:08:28.521490+00:00
pubmed
last seen: 2026-08-23T06:10:08.617328+00:00
scilite
last seen: 2026-08-23T10:03:07.687773+00:00
unpaywall
last seen: 2026-08-23T06:29:45.520198+00:00
License: public-domain-us · commercial use OK · attribution required
Courtesy of the U.S. National Library of Medicine