Dysfunctional signaling underlying endometriosis: current state of knowledge.

Abstract:

: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.

journal_name

J Mol Endocrinol

authors

Cho YJ,Lee SH,Park JW,Han M,Park MJ,Han SJ

doi

10.1530/JME-17-0227

subject

Has Abstract

pub_date

2018-04-01 00:00:00

pages

R97-R113

issue

3

eissn

0952-5041

issn

1479-6813

pii

JME-17-0227

journal_volume

60

pub_type

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