Decoding adenomyosis pathogenesis using an assembloid model

Yiliang Xu, Tao Cheng, Jianzhang Wang, Zhiruo Qiu, Xiaohong Guan, Yayuan Yu, Jiacheng Shen, Fangfang Xu, Xiaohong Jiang, Dandan Bai, Mingzhu Wang, Shuyan Mei, Hong Wang, Xiaocui Xu, Li Wu, Shaorong Gao, Xuan Che
Science China. Life sciences · 2025 · vol. 69(1) , pp. 136–150 · doi:10.1007/s11427-025-2981-1 · PMID:40889046 · W4413874807
article OA: closed CC0 ⤵ 1 in-corpus citation
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⚙ AI-generated summary by claude@2026-06+body, 2026-06-09 ⓘ

An endometrial assembloid model was developed to mimic cycle-dependent responses and adenomyosis hallmarks, revealing altered stromal cell populations and signaling pathways that increase immunity and angiogenesis.

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Abstract

Adenomyosis remains a challenging gynecological disorder to investigate due to the absence of in vitro models that accurately replicate endometrial tissue dynamics across the menstrual cycle. To address this gap, we established an endometrial assembloid model that faithfully mimics cycle-dependent endometrial responses and captures key cellular and molecular hallmarks of adenomyosis, including ectopic lesion- specific epithelial and stromal heterogeneity. Single-cell transcriptomics revealed that ectopic epithelial cells shift toward a luminal- dominant, glandular-deficient transcriptional profile during the secretory-like phase. This transition correlated with ectopic stromal reorganization-specifically, loss of BMP4+ stromal cells and an accumulation of CRYAB+IL15+ stromal cells-which impaired BMP-mediated stromal-epithelial signaling while enhancing WNT activation. Additionally, ectopic epithelial and stromal cells demonstrated increased immunity and angiogenesis activities. Our assembloid platform not only provides a physiologically relevant model for investigating adenomyosis pathogenesis but also implicates aberrant WNT signaling as a potential therapeutic target, offering new opportunities for mechanism-driven treatment strategies.

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Condition tags

adenomyosis

MeSH descriptors

Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Endometrium Endometrium Endometrium

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 (47)

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