The evolution of endometriosis research models: a paradigm shift from immortalized cell lines to organoids†

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This review traces the evolution of endometriosis research models, highlighting the limitations of cell lines and animal models while emphasizing the transformative potential of organoids for disease modeling and personalized therapy.

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Abstract

Endometriosis is a complex condition affecting 10% of reproductive-age women worldwide, yet its study has long been hindered by the shortcomings of traditional research models. This review aims to propose a novel theoretical framework and strategic roadmap to accelerate precision medicine in endometriosis. We systematically trace the evolution of research models in the field and critically assess the inherent constraints of conventional systems, including immortalized cell lines and primary cell cultures. While immortalized lines often fail to capture patient heterogeneity due to genetic drift, animal models cannot fully replicate the human immune microenvironment. Although primary cells preserve patient-specific traits and support personalized drug testing, their two-dimensional culture format limits their ability to mimic the three-dimensional (3D) architecture and dynamic cell-cell interactions of native tissues. Recent breakthroughs in organoid technology are reshaping endometriosis research by enabling 3D structural reconstruction, hormone responsiveness, and simulation of lesion progression. This review highlights the transformative potential of organoids in disease modeling, drug screening, and personalized therapy. We also discuss future opportunities for integrating organoids with emerging platforms-such as organ-on-a-chip systems, multi-omics analyses, and digital twin technology-to open new avenues for understanding disease mechanisms and advancing targeted treatments.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis

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 (83)

Source provenance

europepmc
last seen: 2026-06-12T06:13:51.797165+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
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License: CC0 · commercial use OK