Transgenic mice applications in the study of endometriosis pathogenesis

Yali Zhao, Yao Wang, Pinlang Gu, Lingjin Tuo, Leilei Wang, Shi-Wen Jiang, Shi‐Wen Jiang
Frontiers in cell and developmental biology · 2024 · vol. 12 , pp. 1376414 · doi:10.3389/fcell.2024.1376414 · PMID:38933332 · PMC11199864 · W4399593449
article OA: gold CC0 ⤵ 2 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

Transgenic mice offer versatile tools for endometriosis research, allowing investigation of disease pathogenesis, gene function, and interactions with environmental factors via specific genetic modifications and tissue labeling.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 ⓘ

This paper is a review describing how transgenic mouse models—especially GFP/β-gal–labeled or gene-manipulated uterine/pelvic models combined with uterine tissue transplantation—are used to study endometriosis pathogenesis, including hormonal regulation, angiogenesis, and inflammation. It highlights findings from hormone-focused transgenic knockout experiments such as progesterone receptor (PR) knockout and estrogen receptor α/β knockout models, where hormone treatments after auto- or hetero-transplantation altered ectopic lesion growth, proliferation markers, and lesion characteristics, with explicit caveats that EM mechanisms remain incompletely understood and that model advantages/disadvantages and technical considerations matter. The paper primarily synthesizes prior experimental work rather than presenting new original data and notes that no definitive treatment exists, motivating deeper mechanistic animal studies. This paper is centrally about endometriosis — it reviews transgenic mouse and transplantation-based approaches to define in vivo roles of specific genes and hormonal pathways in endometriosis pathogenesis.

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Abstract

Endometriosis (EM), characterized by ectopic growth of endometrial tissues and recurrent pelvic pain, is a common disease with severe negative impacts on the life quality of patients. Conventional uterine tissue transplantation-based models have been broadly used to investigate the pathogenic mechanism(s) of EM. Transgenic mice with whole body or uterine/pelvic tissue-specific labelling by the expression of GFP, β-gal or other light-emitting or chromogenic markers enable investigators to analyze the contribution to endometriotic lesions by the donor or recipient side after uterine tissue transplantation. Moreover, when coupled to uterine tissue transplantation, transgenic mice with a specific EM-related gene knocked out or overexpressed make it possible to determine the gene’s in vivo role(s) for EM pathogenesis. Furthermore, observations on the rise of de novo endometriotic lesions as well as structural/functional changes in the eutopic endometrium or pelvic tissues after gene manipulation will directly relate the cognate gene to the onset of EM. A major advantage of transgenic EM models is their efficiency for analyzing gene interactions with hormonal, dietetic and/or environmental factors. This review summarizes the features/sources/backgrounds of transgenic mice and their applications to EM studies concerning hormonal regulation, angiogenesis and inflammation. Findings from these studies, the advantages/disadvantages of transgenic EM models, and future expectations are also discussed.

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endometriosis

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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.

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