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<p>The uterine cavity was formerly considered sterile; however, over recent years, researchers have identified the presence of endometrial microbiota. An imbalance in the endometrial microbiota, or dysbiosis, has been shown to be associated with a variety of gynecological diseases. Endometriosis (EM) is a chronic and inflammatory gynecological disease that affects 6–10% of all women of reproductive-age. Previous studies suggested that endometrial dysbiosis can participate in the development of EM by generating an inflammatory state, leading to disorders of immune homeostasis and thus creating an intrauterine environment conducive to endometrial stromal cell migration and adhesion. In this review, we investigate differences in the endometrial microbiota of patients with EM compared with that of healthy women and discuss the possible pathogenic mechanisms responsible for endometrial dysbiosis. Critically, we identified that an increase of lipopolysaccharides resulting from microbiological disorders may generate chronic inflammation, leading to increased adhesion and angiogenesis, and the development of EM. The findings of our review may identify new therapeutic strategies and potential therapeutic targets for EM.</p>

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Advances in the Role of Endometrial Microbiota Alterations in the Pathogenesis of Endometriosis

  • 期刊论文

  • 发表日期：

    2026年2月9日

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  • Ziying Xu,
  • Weina Guo,
  • Yi Shen

摘要

The uterine cavity was formerly considered sterile; however, over recent years, researchers have identified the presence of endometrial microbiota. An imbalance in the endometrial microbiota, or dysbiosis, has been shown to be associated with a variety of gynecological diseases. Endometriosis (EM) is a chronic and inflammatory gynecological disease that affects 6–10% of all women of reproductive-age. Previous studies suggested that endometrial dysbiosis can participate in the development of EM by generating an inflammatory state, leading to disorders of immune homeostasis and thus creating an intrauterine environment conducive to endometrial stromal cell migration and adhesion. In this review, we investigate differences in the endometrial microbiota of patients with EM compared with that of healthy women and discuss the possible pathogenic mechanisms responsible for endometrial dysbiosis. Critically, we identified that an increase of lipopolysaccharides resulting from microbiological disorders may generate chronic inflammation, leading to increased adhesion and angiogenesis, and the development of EM. The findings of our review may identify new therapeutic strategies and potential therapeutic targets for EM.