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Related Experiment Video

Updated: Sep 9, 2025

Establishment of an Experimental Mouse Model of Endometrioma to Study its Related Infertility

Establishment of an Experimental Mouse Model of Endometrioma to Study its Related Infertility

Published on: April 5, 2024

Decoding adenomyosis pathogenesis using an assembloid model.

Yiliang Xu^1,2, Tao Cheng³, Jianzhang Wang⁴

¹Key Laboratory of Animal Bioengineering and Disease Prevention of Shandong Province, College of Animal Science and Technology, Shandong Agricultural University, Tai'an, 271018, China.

Science China. Life Sciences

|September 1, 2025

Summary

This summary is machine-generated.

Researchers developed a novel endometrial assembloid model to study adenomyosis. This model mimics menstrual cycle changes and reveals aberrant WNT signaling in adenomyosis, suggesting a new therapeutic target for this challenging gynecological disorder.

Keywords:

adenomyosis assembloid model single-cell sequencing stromal-epithelial interaction

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Last Updated: Sep 9, 2025

Establishment of an Experimental Mouse Model of Endometrioma to Study its Related Infertility

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A Syngeneic Murine Model of Endometriosis using Naturally Cycling Mice

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Published on: November 24, 2020

Heterotypic Three-dimensional In Vitro Modeling of Stromal-Epithelial Interactions During Ovarian Cancer Initiation and Progression

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Published on: August 28, 2012

Area of Science:

Gynecology
Cell Biology
Tissue Engineering

Background:

Adenomyosis research is hindered by the lack of accurate in vitro models.
Existing models do not fully replicate endometrial tissue dynamics throughout the menstrual cycle.

Purpose of the Study:

To establish a novel endometrial assembloid model for studying adenomyosis.
To investigate the cellular and molecular mechanisms underlying adenomyosis pathogenesis.

Main Methods:

Development of a 3D endometrial assembloid model.
Single-cell transcriptomics to analyze cellular changes.
Analysis of stromal-epithelial signaling pathways.

Main Results:

The assembloid model accurately mimics cycle-dependent endometrial responses and adenomyosis hallmarks.
Ectopic epithelial cells exhibit a luminal-dominant, glandular-deficient profile during the secretory phase.
Stromal reorganization involves loss of BMP4+ cells and gain of CRYAB+IL15+ cells, impairing BMP signaling and activating WNT signaling.
Ectopic cells show increased immunity and angiogenesis.

Conclusions:

The endometrial assembloid platform provides a physiologically relevant model for adenomyosis research.
Aberrant WNT signaling is implicated in adenomyosis pathogenesis and represents a potential therapeutic target.
This model offers new avenues for developing mechanism-driven treatment strategies for adenomyosis.