Hormonal imbalance-mediated immune inflammation in endometrial decidualization disorder

Yu J, Jiaxin Yu, Qin R, Rongyan Qin, Huang P, Pinxiu Huang, Hang F, Fu Hang, F Hang, Yuying Guo, Guo Y, Yanhui Li, Li Y, Yuhua Yang, Yuni Yang, Yang Y, Wu H, Huanhuan Wu, Ying Liu, Liu Y, Ming Liao, Liao M, Qin A, Aiping Qin
Placenta · 2025 · vol. 180 , pp. 111–117 · doi:10.1016/j.placenta.2025.06.025 · PMID:40628562 · W4411919056
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This paper investigates how hormonal imbalances contribute to immune inflammation in disorders of endometrial decidualization.

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Abstract

The dynamic interplay between hormonal signalling and immune-inflammatory homeostasis is pivotal for regulating endometrial decidualization, which is indispensable for successful embryo implantation. Hormonal imbalance-mediated inflammation, particularly the imbalance between oestrogen and progesterone levels, severely disrupts endometrial decidualization. Endometriosis is characterised by oestrogen-progesterone imbalance, which is common in endometrial decidualization disorders. In endometriosis, oestrogen dominance and progesterone resistance disrupt homeostasis through multifaceted pathological mechanisms. Excessive oestrogen activates nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signalling, driving overproduction of pro-inflammatory cytokines and transcriptional suppression of progesterone receptor B (PR-B), thereby impairing stromal cell differentiation. Concurrent progesterone resistance attenuates anti-inflammatory responses, including NF-κB inhibition and interleukin 10 induction, and exacerbates endometrial immune dysregulation. Retinoic acid synthesis impairment and oestrogen-prostaglandin E2 feedback loops sustain a pathological hyperoestrogenic microenvironment, fostering a self-perpetuating cycle of "oestrogen dominance-inflammation-progesterone resistance". Immune disturbances at the maternal-foetal interface, such as classically activated macrophage polarisation, T-helper cell bias, and dysregulated natural killer cell cytotoxicity, further disrupt decidualization by impairing immunotolerance. Therefore, therapeutic strategies targeting these pathways are promising. Dienogest suppresses aromatase/cyclooxygenase-2 (COX-2)-mediated oestrogen synthesis and restores progesterone sensitivity via PR-B upregulation. Immunomodulatory approaches, including corticosteroids and tumour necrosis factor-α inhibitors, improve pregnancy outcomes in endometriosis-associated infertility. Future research, leveraging state-of-the-art technologies, should prioritise elucidating the molecular interactions within the oestrogen-progesterone-immune axis and translating these insights into personalised therapies to optimise the management of decidualization-related disorders.

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MeSH descriptors

Decidua Decidua Decidua Decidua Decidua Decidua Decidua Decidua Decidua Decidua Decidua Decidua Decidua Decidua Decidua Decidua Decidua Decidua Decidua Decidua

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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. Outer rings show 2-hop neighbours — papers reached through the immediate citers/citees. [ collapse to 1-hop ]

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