期刊
JOURNAL OF MOLECULAR ENDOCRINOLOGY
卷 60, 期 3, 页码 R97-R113出版社
BIOSCIENTIFICA LTD
DOI: 10.1530/JME-17-0227
关键词
endometriosis; inflammation; apoptosis; oxidative stress; estrogen receptor
资金
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) [5 U24 DK097748-04]
- Mike Hogg Foundation
- Basic Science Research Program through the National Research Foundation of Korea (NRF) -Ministry of Science, ICT & Future planning [NRF-2016R1C1B1006976]
- Dong-A University Research Fund
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [U24DK097748] Funding Source: NIH RePORTER
Endometriosis is defined as the presence of endometrial tissue outside the uterine cavity. It affects approximately 5-10% of women of reproductive age. Endometriosis is associated with dysmenorrhea, dyspareunia and, often, severe pelvic pain. In addition to pain, women with endometriosis often experience infertility. Defining the molecular etiology of endometriosis is a significant challenge for improving the quality of women's lives. Unfortunately, the pathophysiology of endometriosis is not well understood. Here, we summarize the potential causative factors of endometriosis in the following three categories: (1) dysregulation of immune cells in the peritoneal fluid and endometriotic lesions; (2) alteration of apoptotic signaling in retrograde menstrual tissue and cytotoxic T cells involved in endometriosis progression and (3) dysregulation of oxidative stress. Determining the molecular etiology of these dysregulated cellular signaling pathways should provide crucial clues for understanding initiation and progression of endometriosis. Moreover, improved understanding should suggest new molecular therapeutic targets that could improve the specificity of endometriosis treatments and reduce the side effects associated with current approaches.
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