Endometriosis disease: the patogenetic role of hormone resepters and methods of diagnosis

А. О. Дробинцева, A E Andreev, V. О. Polyakova, I. М. Kvetnoy
In: Clinical Medicine (Russian Journal) · 2018 · vol. 96(9) , pp. 796–803 · doi:10.18821/0023-2149-2018-96-9-796-803 · W3098228360
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This review examines the roles of estrogen, progesterone, prolactin, anti-Müllerian hormone, kisspeptin, and melatonin receptors in endometriosis pathogenesis, highlighting altered expression patterns of ERs, AMHR2, and KISS1R and inconsistent findings for PR and PLR.

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Abstract

This review summarizes current literature data taken from the information bases of elibrary and pubmed, on hormone receptors, which participate or have a significant impact on the pathogenesis of endometrial disease according to new data sources. They include estrogen receptors (ERa; ERe), progesterone receptors (PRA; PRB), prolactin receptors (PLR), anti-mullerian hormone receptor (AMHR2), kisspeptin receptor (KISS1R) and melatonin receptor (MR). It was established that expression of ERe genes is up-regulated in heterotopy, whereas ERa expression is lower compared to normal tissue. The progesterone receptor is of great interest for study because of inconsistent data on its expression. Receptors for anti-mullerian hormone hormone is no less significant in the study of the pathogenesis of the disease, since AMH stimulates apoptosis in endometrioid cells, limiting their expansion. The most controversial role in endometriosis belongs to prolactin receptors, some authors believe that in endometriosis, a decrease in expression of PLR is observed, while in other articles an increase of expression is postulated. It has been shown that in patients with endometriosis, the expression of the KISS1R is reduced in the endometrium. The data on the expression of melatonin and its receptors in endometriosis is absence.

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Condition tags

endometriosis

Citation neighborhood (2-hop)

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. Outer rings show 2-hop neighbours — papers reached through the immediate citers/citees. [ collapse to 1-hop ]

References (19)

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