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子宫腺肌病中蜕膜化异常导致子宫内膜容受性降低的分子机制。

Molecular mechanism of aberrant decidualization in adenomyosis leading to reduced endometrial receptivity.

作者信息

Dai Yuanquan, Yuan Zheng, Fan Weisen, Lin Zhiheng

机构信息

Department of Gynecology, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, Shandong, China.

Department of Gynecology, Guang anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China.

出版信息

Front Endocrinol (Lausanne). 2025 Jan 16;15:1435177. doi: 10.3389/fendo.2024.1435177. eCollection 2024.

DOI:10.3389/fendo.2024.1435177
PMID:39886033
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11779606/
Abstract

Patients with adenomyosis not only experience a decrease in quality of life as a result of dysmenorrhea and severe monthly flow but they are also rendered infertile. Pregnancy rates are still low among women with adenomyosis, even with assisted reproduction. According to the current study, endometrial receptivity is primarily responsible for the lower conception rate among patients with adenomyosis. Decidualization of endometrial stromal cells is the fundamental requirement for endometrial receptivity and the maintenance of a normal pregnancy, even though endometrial receptivity is made up of a variety of cells, including immune cells, endometrial epithelial cells, and endometrial stromal cells. Our overview reveals that endometriosis deficiencies are present in patients with adenomyosis. These flaws may be linked to aberrant pathways in endometrial stromal cells, such as PI3K/Akt, JAK2/STAT3, and hedgehog. Correcting the abnormal expression of molecules in endometrial stromal cells in the endometrium of patients with adenomyosis may become the focus of research to improve endometrial receptivity and increase the pregnancy rate.

摘要

患有子宫腺肌病的患者不仅因痛经和月经过多而生活质量下降,而且还会导致不孕。即使采用辅助生殖技术,子宫腺肌病患者的妊娠率仍然很低。根据目前的研究,子宫内膜容受性是子宫腺肌病患者受孕率较低的主要原因。子宫内膜基质细胞的蜕膜化是子宫内膜容受性和维持正常妊娠的基本要求,尽管子宫内膜容受性由多种细胞组成,包括免疫细胞、子宫内膜上皮细胞和子宫内膜基质细胞。我们的综述显示,子宫腺肌病患者存在子宫内膜容受性缺陷。这些缺陷可能与子宫内膜基质细胞中的异常信号通路有关,如PI3K/Akt、JAK2/STAT3和hedgehog信号通路。纠正子宫腺肌病患者子宫内膜中子宫内膜基质细胞分子的异常表达可能成为提高子宫内膜容受性和增加妊娠率的研究重点。

相似文献

1
Molecular mechanism of aberrant decidualization in adenomyosis leading to reduced endometrial receptivity.子宫腺肌病中蜕膜化异常导致子宫内膜容受性降低的分子机制。
Front Endocrinol (Lausanne). 2025 Jan 16;15:1435177. doi: 10.3389/fendo.2024.1435177. eCollection 2024.
2
Decreased expression of LEF1 caused defective decidualization by inhibiting IL-11 expression in patients with adenomyosis.LEF1表达降低通过抑制子宫腺肌病患者的IL-11表达导致蜕膜化缺陷。
Mol Med. 2025 Jan 10;31(1):10. doi: 10.1186/s10020-024-01054-9.
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Aberrant TCF21 upregulation in adenomyosis impairs endometrial decidualization by increasing PDE4C expression.腺肌病中异常的 TCF21 上调通过增加 PDE4C 的表达来损害子宫内膜蜕膜化。
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Decreased expression of NR4A nuclear receptors in adenomyosis impairs endometrial decidualization.子宫腺肌病中NR4A核受体表达降低会损害子宫内膜蜕膜化。
Mol Hum Reprod. 2016 Sep;22(9):655-68. doi: 10.1093/molehr/gaw042. Epub 2016 Aug 11.
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Scribble downregulation in adenomyosis compromises endometrial stromal decidualization by decreasing FOXO1 expression. scribble 下调在子宫腺肌病中通过降低 FOXO1 表达来损害子宫内膜基质蜕膜化。
Hum Reprod. 2021 Dec 27;37(1):93-108. doi: 10.1093/humrep/deab234.
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CDC42 deficiency leads to endometrial stromal cell senescence in recurrent implantation failure.CDC42缺陷导致反复种植失败中子宫内膜基质细胞衰老。
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Paradoxical role of phosphorylated STAT3 in normal fertility and the pathogenesis of adenomyosis and endometriosis†.磷酸化 STAT3 在正常生育力和子宫腺肌病及子宫内膜异位症发病机制中的矛盾作用†。
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Determining the Molecular Background of Endometrial Receptivity in Adenomyosis.确定子宫腺肌病中子宫内膜容受性的分子背景。
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Generation of epithelial-stromal assembloids as an advanced in vitro model of impaired adenomyosis-related endometrial receptivity.生成上皮-基质组装体作为子宫腺肌病相关子宫内膜容受性受损的先进体外模型。
Fertil Steril. 2025 Feb;123(2):350-360. doi: 10.1016/j.fertnstert.2024.08.339. Epub 2024 Aug 27.
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METTL3-dependent m6A modification facilitates decreased endometrial decidualization via attenuation of MET in endometriosis.METTL3 依赖性 m6A 修饰通过衰减 MET 促进子宫内膜异位症中子宫内膜蜕膜化减少。
Reproduction. 2024 Aug 5;168(3). doi: 10.1530/REP-23-0336. Print 2024 Sep 1.

本文引用的文献

1
Dysregulated expression of GATA2 and GATA6 transcription factors in adenomyosis: implications for impaired endometrial receptivity.GATA2 和 GATA6 转录因子在子宫腺肌病中的失调表达:对子宫内膜容受性受损的影响。
F S Sci. 2024 Feb;5(1):92-103. doi: 10.1016/j.xfss.2023.11.003. Epub 2023 Nov 14.
2
Paradoxical role of phosphorylated STAT3 in normal fertility and the pathogenesis of adenomyosis and endometriosis†.磷酸化 STAT3 在正常生育力和子宫腺肌病及子宫内膜异位症发病机制中的矛盾作用†。
Biol Reprod. 2024 Jan 13;110(1):5-13. doi: 10.1093/biolre/ioad148.
3
Endometrial cell‑derived exosomes facilitate the development of adenomyosis via the IL‑6/JAK2/STAT3 pathway.
子宫内膜细胞衍生的外泌体通过IL-6/JAK2/STAT3信号通路促进子宫腺肌病的发展。
Exp Ther Med. 2023 Sep 26;26(5):526. doi: 10.3892/etm.2023.12225. eCollection 2023 Nov.
4
miR-141-3p Regulates the Proliferation and Apoptosis of Endometrial-Myometrial Interface Smooth Muscle Cells in Adenomyosis Via JAK2/STAT3 Pathway.miR-141-3p 通过 JAK2/STAT3 通路调节子宫腺肌病在位内膜-肌层界面平滑肌细胞的增殖和凋亡。
Biochem Genet. 2024 Jun;62(3):2049-2065. doi: 10.1007/s10528-023-10508-4. Epub 2023 Oct 12.
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PLEKHS1 drives PI3Ks and remodels pathway homeostasis in PTEN-null prostate.PLEKHS1 驱动 PI3Ks 并重塑 PTEN 缺失型前列腺中的通路动态平衡。
Mol Cell. 2023 Aug 17;83(16):2991-3009.e13. doi: 10.1016/j.molcel.2023.07.015. Epub 2023 Aug 10.
6
Adenomyosis: An Updated Review on Diagnosis and Classification.子宫腺肌病:诊断与分类的最新综述
J Clin Med. 2023 Jul 21;12(14):4828. doi: 10.3390/jcm12144828.
7
IHH, SHH, and primary cilia mediate epithelial-stromal cross-talk during decidualization in mice.在小鼠蜕膜化过程中,IHH、SHH和初级纤毛介导上皮-基质间的相互作用。
Sci Signal. 2023 Feb 28;16(774):eadd0645. doi: 10.1126/scisignal.add0645.
8
The Regulators of Human Endometrial Stromal Cell Decidualization.人类子宫内膜基质细胞蜕膜化的调节因子。
Biomolecules. 2022 Sep 10;12(9):1275. doi: 10.3390/biom12091275.
9
Extracellular vesicles secreted by human uterine stromal cells regulate decidualization, angiogenesis, and trophoblast differentiation.人子宫基质细胞分泌的细胞外囊泡调节蜕膜化、血管生成和滋养细胞分化。
Proc Natl Acad Sci U S A. 2022 Sep 20;119(38):e2200252119. doi: 10.1073/pnas.2200252119. Epub 2022 Sep 12.
10
Decreased intracellular IL-33 impairs endometrial receptivity in women with adenomyosis.腺肌病患者子宫内膜容受性降低与细胞内 IL-33 减少有关。
Front Endocrinol (Lausanne). 2022 Jul 22;13:928024. doi: 10.3389/fendo.2022.928024. eCollection 2022.