Increased Expression of YAP Inhibited the Autophagy Level by Upregulating mTOR Signal in the Eutopic ESCs of Endometriosis

Tianjiao Pei, Bin Luo, Tingting Liu, Wei Huang, Dong Liu, Yujing Li, Li Xiao, Xin Huang, Yunwei Ouyang, Huili Zhu
Frontiers in endocrinology · 2022 · vol. 13 , pp. 813165 · doi:10.3389/fendo.2022.813165 · PMID:35173685 · PMC8842667 · W4210419327
article OA: gold CC0 ⤵ 7 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

Overexpression of YAP in endometriosis endometrial stromal cells upregulated mTOR signaling, inhibiting autophagy and impacting decidualization, suggesting a role for the YAP-autophagy axis in endometriosis pathogenesis.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-10 ⓘ

The study investigated how Yes-associated protein (YAP) regulates autophagy and decidualization in eutopic endometrial stromal cells (ESCs) from women with endometriosis, using primary ESC cultures from 12 endometriosis patients and 9 controls, combined with analysis of YAP-associated gene sets from GEO dataset GSE51981. Differential expression and pathway enrichment highlighted the autophagy pathway, and mechanistically, YAP overexpression increased mTOR expression while decreasing LC3-II/LC3-I and other autophagy marker ratios, with fewer autophagosomes observed by transmission electron microscopy; rapamycin-treated ESCs showed increased decidual prolactin after in vitro decidualization. A noted limitation is the relatively small patient sample size (and stratification across phases/stages within the referenced dataset), which constrains how broadly the findings can be generalized. This paper is centrally about endometriosis — it links increased YAP to mTOR-mediated autophagy inhibition in eutopic ESCs and examines downstream effects on decidualization in endometriosis-associated infertility.

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Abstract

We first reported that the Hippo-YAP signaling pathway plays a critical role in the pathogenesis of endometriosis (EMS). Autophagy is also related to the invasion ability of endometrial cells and is involved in the pathogenesis of EMS through multi-levels. However, the precise regulatory mechanism of YAP on autophagy in the eutopic endometrial stromal cells (ESCs) is still unclear. Primary eutopic ESCs of EMS patients ( n = 12) and control patients without EMS ( n = 9) were isolated and cultured to investigate the expressions of YAP and mTOR, the role of YAP in autophagy, and the effect of the YAP-autophagy signal on the decidualization of the eutopic ESCs. Endometriosis-related sequencing data (GSE51981) in the GEO database were used to find the genes significantly correlated with YAP. We found 155 genes with significant differences in the interaction with YAP in EMS from the dataset, and the autophagy pathway was significantly enriched. Following on from our previous studies of YAP knockdown, overexpression of YAP resulted in an increased expression of mTOR and decreased ratio of LC3-II/LC3-I and autophagy markers, in the eutopic ESCs; transmission electron microscope observation also showed fewer autophagosomes compared with the control cells. Furthermore, ESCs of the Rapamycin-treated group showed significant decidual-like changes with significantly increased decidual prolactin level at 72 h after in vitro decidualization. These results demonstrate that the increased YAP inhibited the level of autophagy by upregulating the mTOR signal in the eutopic ESCs of endometriosis. The YAP-autophagy signal plays an important role in the pathogenesis of endometriosis-associated infertility.

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Condition tags

endometriosisinfertility

MeSH descriptors

Endometriosis Endometriosis Autophagy Endometrium Endometrium Female Humans Stromal Cells Stromal Cells Stromal Cells TOR Serine-Threonine Kinases TOR Serine-Threonine Kinases

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