Molecular aspects of development and regulation of endometriosis

Abstract

Endometriosis is a common and painful condition affecting women of reproductive age. While the underlying pathophysiology is still largely unknown, much advancement has been made in understanding the progression of the disease. In recent years, a great deal of research has focused on non-invasive diagnostic tools, such as biomarkers, as well as identification of potential therapeutic targets. In this article, we will review the etiology and cellular mechanisms associated with endometriosis as well as the current diagnostic tools and therapies. We will then discuss the more recent genomic and proteomic studies and how these data may guide development of novel diagnostics and therapeutics. The current diagnostic tools are invasive and current therapies primarily treat the symptoms of endometriosis. Optimally, the advancement of “-omic” data will facilitate the development of non-invasive diagnostic biomarkers as well as therapeutics that target the pathophysiology of the disease and halt, or even reverse, progression. However, the amount of data generated by these types of studies is vast and bioinformatics analysis, such as we present here, will be critical to identification of appropriate targets for further study.

Association of WNT4 polymorphisms with endometriosis in infertile patients

“…Increasing evidence supports endometriosis as a complex polygenic and multifactorial disease, caused by multiple genetic and environmental factors acting in concert [16,17]. Recently, several genome-wide association studies have demonstrated an association between endometriosis and markers located in or near to WNT4 gene [8][9][10].…”

Anti‐Endometriotic Effects of Pueraria Flower Extract in Human Endometriotic Cells and Mice

“…Activated MAPK coordinates diverse cellular activities including cellular metabolism, differentiation, cell cycle, motility, apoptosis, and survival. One of the MAPKs, ERK1/2, has been suggested as a key regulator of the majority of the signalling pathways and cascades associated with the pathogenesis of endometriosis [38]. For example, some factors in the endometriotic milieu such as tumour necrosis factor α (TNFα) and monocyte chemotactic protein-1 (MCP-1) have been shown to regulate ERK signalling in endometriotic cells [39].…”

MicroRNA‐488 inhibits endometrial glandular epithelial cell proliferation, migration, and invasion in endometriosis mice via Wnt by inhibiting FZD7

“…The amount of women with endometriosis during reproductive years reaches 10%, and those who have pelvic or infertility are more likely to suffer from endometriosis . Although, a previous report indicated that the prevalence of endometriosis had decreased in a certain degree, the incidence of endometriosis was higher than several decades ago . A great deal of health‐care resources and persistent therapy are needed for the patients with endometriosis, since once the current medical therapies are discontinued, the alleviative symptoms are likely to recur and extra interventions are required .…”