Research progress on the correlation between microbiota and endometriosis

Jingyi Wang, Wang J, Wang X, Xiaojie Wang
European journal of obstetrics, gynecology, and reproductive biology · 2025 · vol. 314 , pp. 114671 · doi:10.1016/j.ejogrb.2025.114671 · PMID:40865134
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⚙ AI-generated summary by claude@2026-06, 2026-06-13 ⓘ

This review summarizes current research on how gut and reproductive tract microbiota dysbiosis contributes to the pathogenesis of endometriosis through inflammation.

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Abstract

The microbiota constitutes a vital component of the human microenvironment, dynamically responding to physiological changes and playing crucial roles in maintaining normal bodily functions. Endometriosis (EMs), defined as a chronic, hormone-dependent inflammatory disorder, involves the ectopic implantation of endometrium-like tissue beyond the uterine cavity (e.g., ovaries, peritoneum). This pathology initiates local and systemic inflammatory cascades, leading to characteristic clinical manifestations such as dysmenorrhea (occurring in ∼ 84.9 % of patients), chronic pelvic pain, infertility, and psychological comorbidities. Emerging evidence suggests that dysbiosis in both gut and reproductive tract microbiota can initiate local immune inflammatory responses, which subsequently propagate systemic inflammation via cytokine networks and metabolic pathways, thereby contributing to EMs pathogenesis. Microbiota-targeted interventions have recently emerged as a promising diagnostic and therapeutic strategy. This review systematically summarizes current advances in understanding microbiota dysbiosis-EMs interactions, aiming to provide new insights for developing innovative management approaches.

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Condition tags

endometriosischronic_pelvic_paindysmenorrheainfertility

MeSH descriptors

Dysbiosis Dysbiosis Dysbiosis Dysbiosis Dysbiosis Dysbiosis Dysbiosis Dysbiosis Dysbiosis Dysbiosis Dysbiosis Dysbiosis Dysbiosis Dysbiosis Dysbiosis Dysbiosis Dysbiosis Dysbiosis Dysbiosis Dysbiosis

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 (62)

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