Negative impacts of ovarian endometrioma on preantral follicle development: implications for endometriosis-related infertility

Makoto Orisaka, Aya Shirafuji, Natsumi Shimizu-Mizuno, Miki Uesaka, Yūkō Fujita, Katsutoshi Mizuno, Masayuki Fujita, Yumiko Miyazaki, Toshimichi Onuma, Hideaki Tsuyoshi, Tetsuya Mizutani, Benjamin K. Tsang, Yoshio Yoshida
In: Frontiers in Endocrinology · 2026 · vol. 17 , pp. 1679042 · doi:10.3389/fendo.2026.1679042 · PMID:42199791 · W7160860317
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⚙ AI-generated summary by claude@2026-06, 2026-06-06 ⓘ

Endometrioma fluid impairs preantral follicle development by inducing oxidative stress in granulosa cells and fibrosis in theca cells, disrupting their communication.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-06 ⓘ

The paper studied how pooled endometrioma fluid from six endometrioma patients affects rat preantral follicle development in vitro, using isolated 14-day-old rat preantral follicles cultured with or without endometrioma fluid concentrations and FSH, then assessing follicle growth, steroid production, marker gene expression, oxidative stress (ROS), and fibrotic changes. The key findings were that endometrioma fluid inhibited granulosa cell proliferation, reduced FSH-stimulated estradiol production, and downregulated granulosa markers including FSH receptor, anti-Müllerian hormone, and aromatase, while also promoting theca cell proliferation and inducing oxidative stress and fibrotic marker expression (including TGF-β1 and collagen type III) that could impair granulosa–theca crosstalk. Potential protective agents (antioxidants, antifibrotic drugs, and iron chelators) did not show significant effects, whereas androgen supplementation partially restored granulosa cell proliferation and FSH receptor expression. A major limitation is that all mechanistic experiments were performed in a rat preantral follicle culture system exposed to filtered pooled endometrioma fluid rather than in human follicles in vivo. This paper is centrally about endometriosis — ovarian endometrioma fluid was shown to disrupt preantral follicle development through oxidative stress and fibrosis mechanisms relevant to endometriosis-related infertility.

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Abstract

Background: Endometriosis is a chronic, estrogen-dependent inflammatory disorder and a leading cause of female infertility. Ovarian endometriomas, a common manifestation of endometriosis, are commonly associated with diminished ovarian function; however, the mechanisms underlying endometrioma-induced follicular dysregulation remain poorly understood. Thus, we aimed to determine whether endometrioma fluid (EmF) compromises preantral follicle development via oxidative stress and tissue fibrosis. Methods: EmF was collected from six patients during laparoscopic cystectomy or transvaginal ethanol sclerotherapy for endometriomas. Large preantral follicles (diameter: 130-160 µm) were isolated from 14-day-old rats and cultured in the presence or absence of 0.5% EmF and 10 ng/mL follicle-stimulating hormone (FSH). Follicular growth, steroidogenesis, and the expression of granulosa cell (GC) and theca cell (TC) markers were evaluated using morphometric analysis, hormone assays, and quantitative real-time PCR. Oxidative stress and fibrosis were assessed by measuring intracellular reactive oxygen species (ROS) levels and by performing immunostaining for fibrosis markers. In addition, the potential protective effects of pharmacological agents, including antioxidants, antifibrotic drugs, iron chelators, and androgens, were investigated. Results: EmF inhibited GC proliferation, suppressed FSH-induced estradiol production, and downregulated the expression of FSH receptor, anti-Müllerian hormone, and aromatase. Conversely, EmF promoted TC proliferation while downregulating LH receptor expression and androgenic enzyme levels. EmF also increased ROS generation in GC and induced the expression of the fibrotic markers, including transforming growth factor beta 1 and collagen type III, in TC. Androgen supplementation partially restored GC proliferation and FSH receptor expression, whereas antioxidants, antifibrotic agents, and iron chelators showed no significant effects. Conclusions: EmF disrupts preantral follicle development by inducing oxidative stress in GC and promoting fibrosis in TC, thereby impairing GC-TC crosstalk. These findings reveal a novel pathogenic mechanism underlying endometrioma-associated infertility and underscore the need for therapeutic strategies targeting both oxidative stress and fibrotic remodeling within the ovaries.

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Condition tags

endometriosisendometriomainfertility

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References (45)

SciLite annotations

chemicals 8
estrogen ethanol oxygen iron androgen estradiol androgen iron
organisms 1
rattus sp.

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