Impact of Gut and Reproductive Tract Microbiota on Estrogen Metabolism in Endometriosis

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Gut and reproductive tract microbiota regulate estrogen metabolism through mechanisms like beta-glucuronidase activity, influencing endometriosis development by altering metabolites and immune microenvironment.

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This paper is a narrative review examining how gut and reproductive tract microbiota influence estrogen metabolism and thereby relate to the development and progression of endometriosis, integrating evidence on microbial mechanisms such as β-glucuronidase activity, short-chain fatty acid and lipopolysaccharide metabolites, and associated immune microenvironment changes. It also describes a bidirectional relationship in which microbial alterations can drive estrogen imbalance, while fluctuations in estrogen levels can feed back on microbial community composition. The authors state a key caveat that they did not generate or analyze new datasets because the review provides synthesized background rather than original experimental results. Relevance to endometriosis: the paper is centrally about endometriosis and specifically focuses on how microbiota regulate estrogen metabolism (including β-glucuronidase) to influence endometriosis development and progression.

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Abstract

BACKGROUND: The incidence of endometriosis is rising, particularly among younger populations, yet current diagnostic and therapeutic approaches remain limited. This highlights the urgent need for novel diagnostic tools and effective treatments. Recent studies have shown that intestinal and reproductive tract bacterial dysbiosis is closely associated with the development of endometriosis and plays a key role in the regulation of estrogen metabolism. OBJECTIVES: This review aims to provide a comprehensive overview of the mechanisms of the microbiota's role in regulating estrogen levels and influencing the development and progression of endometriosis, providing important insights into the diagnosis and management of the disease. CONCLUSIONS: Microbial changes not only promote estrogen imbalance by regulating β-glucuronidase activity, but also respond to estrogen imbalance by affecting the expression of metabolites such as short-chain fatty acids and lipopolysaccharides. In addition, significant fluctuations in estrogen levels also affect the composition of the microbial community. Both factors jointly lead to changes in the immune microenvironment of endometriosis.
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Background

The incidence of endometriosis is rising, particularly among younger populations, yet current diagnostic and therapeutic approaches remain limited. This highlights the urgent need for novel diagnostic tools and effective treatments. Recent studies have shown that intestinal and reproductive tract bacterial dysbiosis is closely associated with the development of endometriosis and plays a key role in the regulation of estrogen metabolism.

Objectives

This review aims to provide a comprehensive overview of the mechanisms of the microbiota's role in regulating estrogen levels and influencing the development and progression of endometriosis, providing important insights into the diagnosis and management of the disease.

Conclusions

Microbial changes not only promote estrogen imbalance by regulating β-glucuronidase activity, but also respond to estrogen imbalance by affecting the expression of metabolites such as short-chain fatty acids and lipopolysaccharides. In addition, significant fluctuations in estrogen levels also affect the composition of the microbial community. Both factors jointly lead to changes in the immune microenvironment of endometriosis. Conflicts of Interest The authors declare that no conflict of interest is reported in this paper. Data Availability Statement Data sharing not applicable to this article as no datasets were generated or analyzed during the current study.

References

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last seen: 2026-08-24T06:08:07.662257+00:00
pubmed
last seen: 2026-08-24T06:04:42.073416+00:00
unpaywall
last seen: 2026-05-11T08:34:28.763810+00:00
License: public-domain-us · commercial use OK · attribution required
Courtesy of the U.S. National Library of Medicine