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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.

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。

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