Single-cell transcriptomic atlas of ovarian endometriosis patient's follicular fluid: unraveling novel insights into abnormal follicular development

Zhang M, Meng Zhang, Xinye Hu, Hu X, HR Lin, Haiyan Lin, Lin H, Yang Gang, Gang Yang, Gang Y, Yang G, Ji X, Xiaohui Ji, Yaoqiu Wu, Wu Y, Chunwei Cao, Cao C, Yabin Guo, Guo Y, Zhang Q, Qingxue Zhang, Q. Zhang
Reproduction (Cambridge, England) · 2026 · vol. 172(1) · doi:10.1093/reprod/xaag083 · PMID:42411754 · W7167608706
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This single-cell transcriptomic study of ovarian endometriosis follicular fluid identified a novel macrophage subtype and revealed abnormal granulosa cell development, heightened immune inflammation, and altered cell signaling pathways.

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Abstract

In brief: We present the first single-cell transcriptomic atlas of follicular fluid from an ovarian endometrioma (OMA) patient, revealing a novel TCR+ macrophage subtype, aberrant granulosa cell developmental trajectories, immune dysregulation, and enhanced MIF/MK signaling, providing new insights into mechanisms underlying impaired follicular development in OMA. Abstract: Ovarian endometrioma (OMA), an endometriosis subtype, involves hemorrhagic cysts formed by ectopic endometrial-like tissue, causing pelvic pain, inflammation, and infertility by disrupting ovarian function. Despite its impact, the single-cell dynamics in OMA follicular fluid are poorly understood. We performed single-cell RNA sequencing (10x Genomics) on follicular fluid from a patient's affected (2,793 cells) and unaffected (4,699 cells; control) ovaries. Analysis revealed four cell types, including a novel TCR+ macrophage subtype. Affected-side granulosa cells showed abnormal developmental trajectories linked to dysregulated steroid pathways. Immune cells exhibited heightened inflammation and reduced macrophage phagocytosis. Cell-cell communication highlighted prominent Macrophage Migration Inhibitory Factor and Midkine signaling from granulosa cells. This study provides the first single-cell transcriptomic profile of OMA follicular fluid, elucidating aberrant granulosa cell development, immune dysregulation, and distinctive cellular interactions, enhancing understanding of OMA's impact on follicular development and suggesting potential diagnostic/therapeutic targets.

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MeSH descriptors

Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis

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References (55)

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