Targeting HSP90 as a therapeutic approach for endometriosis: insights from proteomic analysis

Jiayu Lin, Weie Zhao, Manchao Li, Mingxin Liu, Liu Mingxin, Qi Guo, Taibao Wu, Yuting Xiang, Jiawen Liu, Yanyan Zeng, Qiqi Liang, Xiaoyan Liang, Chuanchuan Zhou, Jingjie Li
Reproduction (Cambridge, England) · 2026 · vol. 171(2) · doi:10.1093/reprod/xaaf002 · PMID:41643215 · W7124308421
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

This study investigated HSP90 inhibition with 17-AAG in endometriosis models, finding it reduced lesion growth and cell viability while altering key protein networks.

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Abstract

Endometriosis, a chronic inflammatory condition characterized by pain and infertility, remains a clinical challenge. Current hormonal and surgical treatments are often limited by side effects and high recurrence rates. In search of more effective and less invasive alternatives, we analyzed a single-cell RNA sequencing dataset of menstrual effluents from patients (GSE203191) and identified a significant upregulation of heat shock protein 90 (HSP90), suggesting its pathogenic involvement. Using primary endometrial stromal cells (ESCs) isolated from human ovarian endometrioma and a murine endometriosis model, we evaluated the therapeutic potential of HSP90 inhibition with 17-allylamino-17-demethoxygeldanamycin (17-AAG). In vitro, 17-AAG (10 nM-10 μM) reduced ESC viability and proliferation in a dose-dependent manner while increasing caspase-3 activity. In vivo, 17-AAG (30 μg/g) significantly attenuated ectopic lesion growth without impairing systemic parameters such as body weight, anti-Müllerian hormone, or estrogen levels. Proteomic profiling revealed disruption of HSP90 client networks, including downregulation of importin 4 and tubulin gamma complex protein 3, and upregulation of DnaJ heat shock protein family member B1, glutamate-ammonia ligase, and sequestosome 1. These findings highlight HSP90 as a promising non-hormonal therapeutic target in endometriosis, offering mechanistic insights and translational potential for more targeted, well-tolerated treatment strategies.

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Condition tags

mesh:D004715endometriosisendometriomainfertility

MeSH descriptors

Benzoquinones Benzoquinones Benzoquinones Benzoquinones Benzoquinones Benzoquinones Benzoquinones Benzoquinones Benzoquinones Benzoquinones Benzoquinones Benzoquinones Benzoquinones Benzoquinones Benzoquinones Benzoquinones Benzoquinones Benzoquinones Benzoquinones Benzoquinones

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 (53)

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