Impaired fertility in adenomyosis: a murine model reveals endometrial receptivity and progesterone resistance imbalances

Marlyne Squatrito, Julie Vervier, Jules Bindels, Laëtitia Bernet, Silvia Blacher, Michelle Nisolle, Carine Munaut
Reproduction (Cambridge, England) · 2024 · vol. 167(5) · doi:10.1530/rep-24-0019 · PMID:38451875 · W4392563117
article OA: hybrid CC0 ⤵ 8 in-corpus citations
📄 Open PDF View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

This study used a murine model to show that adenomyosis causes subfertility by disrupting estrous cyclicity, folliculogenesis, progesterone receptor expression, and endometrial receptivity.

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

Abstract

In brief: The impact of adenomyosis on reproductive health needs to be fully understood. By using a murine model, this study provides novel insights into the nuanced mechanisms associated with fertility challenges and offers a foundation for targeted interventions. Abstract: This study investigates the intricate relationship between adenomyosis and reproductive health using a murine model, offering novel insights into this prevalent gynecological disorder. Adenomyosis, characterized by the invasive growth of endometrial tissue into the myometrium, is believed to negatively impact fertility. However, the challenge lies in disentangling this influence, as adenomyosis often coexists with other gynecological diseases. A tamoxifen-induced mice model presents a significant advantage by enabling the specific study of adenomyosis, devoid of confounding influences of concurrent gynecological diseases such as endometriosis. Focusing exclusively on adenomyosis, our study aims to elucidate pathogenic mechanisms underlying fertility issues, focusing on estrous cyclicity, ovarian follicle development, and overall fertility. Our findings uncover disruptions in estrous cyclicity, characterized by an increased duration of time spent in the estrus phase in adenomyosis-induced mice. These disturbances are potentially linked to observed compromised folliculogenesis and the remarkable reduction in litter number and size in mice affected by adenomyosis. Moreover, this study unveils potential drivers of subfertility such as progesterone resistance and altered endometrial receptivity. Within the uteri of mice with adenomyosis, reduced expression of the progesterone receptor and a decreased expression of two implantation-related markers (HoxA10 and integrin β3) were observed. This comprehensive examination sheds light on the nuanced complexities of adenomyosis-associated reproductive challenges, providing a foundation for targeted interventions in addressing fertility issues related to this disease.

My notes (saved in your browser only)

Condition tags

mesh:D004715endometriosisadenomyosis

MeSH descriptors

Adenomyosis Adenomyosis Adenomyosis Endometriosis Endometriosis Endometriosis Endometriosis Endometrium Uterine Diseases Uterine Diseases Uterine Diseases Uterine Diseases Animals Animals Animals Disease Models, Animal Disease Models, Animal Disease Models, Animal 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 (88)

Cited by (8)

Source provenance

europepmc
last seen: 2026-06-04T01:30:01.192114+00:00
openalex
last seen: 2026-06-04T00:00:01.174412+00:00
pubmed
last seen: 2026-05-16T00:32:47.498474+00:00
License: CC0 · commercial use OK