ArticleCommunications biology2023
SMAD2/3 signaling in the uterine epithelium controls endometrial cell homeostasis and regeneration.
Article in Communications biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 15 citations in OpenAlex.
- Endometrial cells with high ALDH activity contribute to uterine development and regeneration.eLife · 2026Article
- Endometrial cells with high ALDH activity contribute to uterine development and regeneration.Research square · 2026Article
- Molecular mechanisms and multi-organ regulatory roles of anti-Müllerian hormone in female reproduction.Communications biology · 2026Review
- Multimodal data analysis reveals asynchronous aging dynamics across female reproductive organs.Nature aging · 2026Article
- TGFBR2 coordinates the endometrial response to estrogen, regulating endometrial hyperplasia and fertility.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Transcriptional coregulator ZMIZ1 modulates estrogen responses that are essential for healthy endometrial function.The Journal of clinical investigation · 2025Article
- WERF Endometriosis Phenome and Biobanking Harmonisation Project for Experimental Models in Endometriosis Research (EPHect-EM-Organoids): endometrial organoids as an emerging technology for endometriosis research.Molecular human reproduction · 2025Review
- Integral Roles of the TGFβ Signaling Pathway in Uterine Function and Disease.Endocrinology · 2025Review
- Retinoic acid antagonizes estrogen signaling to maintain adult uterine cell fate.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Bioengineering approaches for the endometrial research and application.Materials today. Bio · 2024Review
- Impaired bone morphogenetic protein (BMP) signaling pathways disrupt decidualization in endometriosis.Communications biology · 2024Article
- Endometrial TGFβ signaling fosters early pregnancy development by remodeling the fetomaternal interface.American journal of reproductive immunology (New York, N.Y. : 1989) · 2023Review
- Impaired bone morphogenetic protein (BMP) signaling pathways disrupt decidualization in endometriosis.Research square · 2023Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
The regenerative potential of the endometrium is attributed to endometrial stem cells; however, the signaling pathways controlling its regenerative potential remain obscure. In this study, genetic mouse models and endometrial organoids are used to demonstrate that SMAD2/3 signaling controls endometrial regeneration and differentiation. Mice with conditional deletion of SMAD2/3 in the uterine epithelium using Lactoferrin-iCre develop endometrial hyperplasia at 12-weeks and metastatic uterine tumors by 9-months of age. Mechanistic studies in endometrial organoids determine that genetic or pharmacological inhibition of SMAD2/3 signaling disrupts organoid morphology, increases the glandular and secretory cell markers, FOXA2 and MUC1, and alters the genome-wide distribution of SMAD4. Transcriptomic profiling of the organoids reveals elevated pathways involved in stem cell regeneration and differentiation such as the bone morphogenetic protein (BMP) and retinoic acid signaling (RA) pathways. Therefore, TGFβ family signaling via SMAD2/3 controls signaling networks which are integral for endometrial cell regeneration and differentiation.
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Registered trials
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