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Pathological functions of hypoxia in endometriosis
Kuei-Yang Hsiao1,Shih-Chieh Lin1,Meng-Hsing Wu1,2,Shaw-Jenq Tsai1,*
1
Department of Physiology, College of Medicine, College of Medicine and Hospital, National Cheng Kung University, Tainan 70101, Taiwan,
2
Department of Obstetrics and Gynecology, College of Medicine and Hospital, National Cheng Kung University, Tainan 70101, Taiwan
DOI: 10.2741/E736 Volume 7 Issue 2, pp.352-366
Published: 01 January 2015
(This article belongs to the Special Issue Frontiers in endometriosis)
*Corresponding Author(s):  
Shaw-Jenq Tsai
E-mail:  
seantsai@mail.ncku.edu.tw
Abstract

Endometriosis is one of the most common gynecological diseases that significantly reduce the life quality of affected women. Research results from the past decade clearly demonstrated that aberrant production of estrogen and cyclooxygenase-2-derived prostaglandin E2 play indispensable roles in the pathogenesis of this disease. However, the etiology of endometriosis remains obscure. Recent evidence reveals a new facet of endometriotic pathogenesis by showing that hypoxia induces the expression of many important downstream genes to regulate the implantation, survival, and maintenance of ectopic endometriotic lesions. These new findings shed lights on future investigations of delineating the etiology of endometriosis and designing new therapeutic strategy for endometriosis.

Key words
HIF-1α,Endometriosis,Prostaglandin,Cyclooxygenase,Leptin,Angiogenesis,Review
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Kuei-Yang Hsiao, Shih-Chieh Lin, Meng-Hsing Wu, Shaw-Jenq Tsai. Pathological functions of hypoxia in endometriosis. Frontiers in Bioscience-Elite. 2015. 7(2); 352-366.