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转录因子如何调节子宫内膜异位症中的细胞凋亡(综述)。

How transcription factors regulate apoptosis in endometriosis (Review).

作者信息

Ouyang Zhuqing, Deng Juexiao, Zhang Lanyue, Shen Fujin

机构信息

Department of Gynaecology and Obstetrics, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.

出版信息

Mol Med Rep. 2025 Nov;32(5). doi: 10.3892/mmr.2025.13654. Epub 2025 Aug 24.


DOI:10.3892/mmr.2025.13654
PMID:40849823
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12382432/
Abstract

Endometriosis (EM) is a common chronic gynaecological disease that affects 10% of women of reproductive age globally. EM is defined as the presence of endometrial glands and stroma in extrauterine locations, and it can result in pelvic pain and infertility. Inflammation, oxidative stress and apoptosis dysregulation serve a key role in endometriotic lesions. The pathogenesis of EM remains unclear, posing major clinical challenges in its diagnosis and treatment. Apoptosis contributes to the maintenance of cellular homeostasis during the menstrual cycle by eliminating ageing cells from the functional layer of the uterine endometrium. Inhibition of apoptosis facilitates ectopic endometrial cell invasion, implantation and survival, and it promotes the occurrence and development of EM. Transcription factors are pivotal regulators of cellular processes and serve key roles in regulating apoptosis to promote EM. Therefore, identifying the mechanisms by which transcription factors regulate apoptosis in EM may help identify novel targets for the treatment of this disease. The present review summarizes the regulation of apoptosis by different transcription factors in the pathogenesis of EM, contributing to the development of promising biomarkers and therapeutic strategies.

摘要

子宫内膜异位症(EM)是一种常见的慢性妇科疾病,全球10%的育龄女性受其影响。EM的定义为子宫外出现子宫内膜腺体和间质,可导致盆腔疼痛和不孕。炎症、氧化应激和凋亡失调在子宫内膜异位病变中起关键作用。EM的发病机制尚不清楚,给其诊断和治疗带来了重大临床挑战。凋亡通过从子宫内膜功能层清除衰老细胞,有助于在月经周期中维持细胞内环境稳定。凋亡抑制促进异位子宫内膜细胞的侵袭、植入和存活,并促进EM的发生和发展。转录因子是细胞过程的关键调节因子,在调节凋亡以促进EM方面起关键作用。因此,确定转录因子在EM中调节凋亡的机制可能有助于识别该疾病治疗的新靶点。本综述总结了不同转录因子在EM发病机制中对凋亡的调节作用,有助于开发有前景的生物标志物和治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3582/12382432/edbbbea2ce62/mmr-32-05-13654-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3582/12382432/05217e836267/mmr-32-05-13654-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3582/12382432/845845e92c59/mmr-32-05-13654-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3582/12382432/edbbbea2ce62/mmr-32-05-13654-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3582/12382432/05217e836267/mmr-32-05-13654-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3582/12382432/845845e92c59/mmr-32-05-13654-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3582/12382432/edbbbea2ce62/mmr-32-05-13654-g02.jpg

相似文献

[1]
How transcription factors regulate apoptosis in endometriosis (Review).

Mol Med Rep. 2025-11

[2]
The Regulation of MicroRNA-21 by Interleukin-6 and Its Role in the Development of Fibrosis in Endometriotic Lesions.

Int J Mol Sci. 2024-8-19

[3]
Expression of lncRNA NEAT1 in endometriosis and its biological functions in ectopic endometrial cells as mediated via miR-124-3p.

Genes Genomics. 2022-5

[4]
Role of Transcription Factor, LIM Homeobox 9 (LHX9) in Inflammatory Response by PGE2 and Thrombin in SERPINA1-Silencing Endometrial Stromal Cells.

Mol Reprod Dev. 2025-8

[5]
Transcription factor EB-mediated autophagy affects cell migration and inhibits apoptosis to promote endometriosis.

Apoptosis. 2024-6

[6]
Endometrial biomarkers for the non-invasive diagnosis of endometriosis.

Cochrane Database Syst Rev. 2016-4-20

[7]
Decreased expression of KLF6 in ectopic endometrial stromal cells contributes to endometriosis progression by targeting CTNNB1.

Cell Signal. 2024-8

[8]
Thymic stromal lymphopoietin contributes to endometriotic lesion proliferation and disease-associated inflammation.

J Immunol. 2025-2-24

[9]
The miRNA Mirage: How Close Are We to Finding a Non-Invasive Diagnostic Biomarker in Endometriosis? A Systematic Review.

Int J Mol Sci. 2018-2-17

[10]
Endometrial alterations in endometriosis: a systematic review of putative biomarkers.

Hum Reprod Update. 2011-6-13

本文引用的文献

[1]
Endometriosis: A Review.

JAMA. 2025-5-5

[2]
OTUD1 inhibits endometriosis fibrosis by deubiquitinating MADH7.

Mol Hum Reprod. 2025-4-3

[3]
Molecular Basis of Impaired Decidualization in the Eutopic Endometrium of Endometriosis Patients.

Cells. 2025-2-21

[4]
Research progress of HIF-1a on immunotherapy outcomes in immune vascular microenvironment.

Front Immunol. 2025-2-6

[5]
MEIS1-mediated Apoptosis via TNFR1 in Endometriosis.

Reprod Sci. 2025-3

[6]
Apoptosis in Cancer Biology and Therapy.

Annu Rev Pathol. 2025-1

[7]
FOXL2 Knockdown Inhibits the Progression of Endometriosis.

Am J Reprod Immunol. 2025-1

[8]
Endometriosis: Future Biological Perspectives for Diagnosis and Treatment.

Int J Mol Sci. 2024-11-14

[9]
Advances in research on malignant transformation of endometriosis-associated ovarian cancer.

Front Oncol. 2024-10-9

[10]
The role of fibrosis in endometriosis: a systematic review.

Hum Reprod Update. 2024-12-1

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