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February 2, 2026Frontiers in Cellular and Infection Microbiology0 citationsOpen Access

Gut microbiota as a key regulator in endometriosis: mechanisms, therapeutic opportunities, and future perspectives

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XLXi LiuMFMinghui FanYWYang Wang

Key Points

  • The research explores the relationship between gut microbiota dysbiosis and the pathogenesis of endometriosis, aiming to inform treatment strategies.
  • Review of existing literature on gut microbiota and endometriosis
  • Analysis of immunoinflammatory and metabolic pathways
  • Evaluation of dietary and microbiota-based interventions
  • Gut microbiota dysbiosis is linked to the progression of endometriosis.
  • Specific metabolic pathways, such as estrogen and lipid metabolism, are influenced by gut microbiota.
  • Dietary changes and probiotics may alleviate symptoms of endometriosis.

Abstract

Endometriosis (EMs), a common and frequently occurring gynecological disease, is a major cause of chronic pelvic pain and infertility in women. Its pathogenesis remains unclear to date, and it is characterized by high invasiveness and recurrence tendency. Although the specific pathogenesis of EMs has not been clarified, existing studies have confirmed that gut microbiota dysbiosis plays an important role in its pathogenic process. Studies suggest that gut microbiota may affect the occurrence and progression of EMs through immunoinflammatory pathways and metabolic pathways (such as enhanced estrogen metabolism and abnormal lipid metabolism). Meanwhile, approaches including dietary intervention, supplementation of probiotics or prebiotics, and microbiota transplantation can help prevent and alleviate EMs symptoms, providing potential therapeutic methods. This article will review the research progress on the correlation between gut microbiota dysbiosis and EMs, with the aim of offering more references for the diagnosis and treatment of EMs.

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Cite This Study

Liu et al. (2026) studied this question.

synapsesocial.com/papers/6980fe13c1c9540dea80fe75https://doi.org/10.3389/fcimb.2025.1730739
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