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Review
. 2023 Feb 24;13(3):430.
doi: 10.3390/biom13030430.

Towards a Better Understanding of Endometriosis-Related Infertility: A Review on How Endometriosis Affects Endometrial Receptivity

Jing Shan  1 , Da-Jin Li  1   2 , Xiao-Qiu Wang  1
Affiliations
Review

Towards a Better Understanding of Endometriosis-Related Infertility: A Review on How Endometriosis Affects Endometrial Receptivity

Jing Shan et al. Biomolecules. .

Abstract

Endometriosis is the most common cause of infertility. Endometrial receptivity has been suggested to contribute to infertility and poor reproductive outcomes in affected women. Even though experimental and clinical data suggest that the endometrium differs in women with endometriosis, the pathogenesis of impaired endometrial receptivity remains incomplete. Therefore, this review summarizes the potential mechanisms that affect endometrial function and contribute to implantation failure. Contemporary data regarding hormone imbalance, inflammation, and immunoregulatory dysfunction will be reviewed here. In addition, genetic, epigenetic, glycosylation, metabolism and microRNA in endometriosis-related infertility/subfertility will be summarized. We provide a brief discussion and perspectives on their future clinical implications in the diagnosis and therapy to improve endometrial function in affected women.

Keywords: endometrial receptivity; endometriosis; epigenetic; glycosylation; immunoregulatory; inflammation; microRNA.

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Conflict of interest statement

The authors have no relevant financial or non-financial interest to disclose.

Figures

Figure 1
Figure 1
Schematic illustration of the mechanism of progesterone and estrogen signaling in the regulation of endometrial receptivity. In the normal endometrium, progesterone and estrogen signaling work together to inhibit epithelial proliferation and facilitate the transition to an embryo-receptive state during the window of implantation. Yet in EMS, the dysfunctions of progesterone and estrogen signaling bring about progesterone resistance and estrogen dominance. ARIDIA, AT-rich interacting domain protein 1A; BCL6, B-cell lymphoma 6; BMP2, bone morphogenetic protein 2; COUP-TFII, chicken ovalbumin upstream transcription factor II; E2, estrogen; ER, estrogen receptor; ERK, extracellular signal-regulated kinase; FGF, fibroblast growth factor; FOXO1, forkhead box O; HAND2, heart- and neural crest derivatives-expressed 2; IHH, Indian Hedgehog; MIG-6, mitogen-induced gene-6; P4, progesterone; PR, progesterone receptor; SIRT1, sirtuin1; Wnt4, wingless-related MMTV integration site4.
Figure 2
Figure 2
The effects of inflammation on endometrium in women with EMS. EMS, endometriosis; IL, interleukin; LIF, leukemia inhibitory factor; TGF, transforming growth factor; TNF, tumor necrosis factor.
Figure 3
Figure 3
Schematic presentation of the endometrial immune environment of women with EMS. CSF, colony-stimulating factor; CXCL, chemokine (C-X-C motif) ligand; DC, dendritic cell; EMS, endometriosis; G-CSF, granulocyte-colony stimulating factor; IDO, indoleamine 23 dioxygenase; IL, interleukin; LIF, leukemia inhibitory factor; NK, natural killer; VEGF, vascular endothelial growth factor; TGF, transforming growth factor; TNF, tumor necrosis factor.
Figure 4
Figure 4
A summary of the pathogenesis of EMS affecting endometrial receptivity.
See this image and copyright information in PMC

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