Estrogen biosynthesis and signaling in endometriosis

Kaisa Huhtinen, Mia Ståhle, Antti Perheentupa, Perheentupa A, Matti Poutanen
Molecular and cellular endocrinology · 2011 · vol. 358(2) , pp. 146–154 · doi:10.1016/j.mce.2011.08.022 · PMID:21875644 · W1976085030
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This paper reviews the roles of estrogen biosynthesis and signaling pathways in the development and progression of endometriosis.

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Abstract

Endometriosis is an estrogen-dependent gynecological disease where endometrium-like tissue grows outside uterine cavity. Endometriotic cell proliferation is stimulated by estrogens acting predominantly via their nuclear receptors. Estrogen receptors (ESR1, ESR2) are ligand activated transcription factors whose activation is dependent on the cell-specific dynamic expression of the receptors, on the interacting proteins and on the ligand availability. The different types of endometriotic lesions, peritoneal, deep, and ovarian endometriosis, may respond to estrogens differentially due to differences in the expression of the receptors and interacting proteins, and due to potential differences in the ligand availability regulated by the local estrogen synthesis. This review summarizes the current knowledge of estrogen synthesizing enzymes and estrogen receptors in different types of endometriosis lesions. Further studies are still needed to define the possible differences in steroid metabolism in different types of endometriotic lesions.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Estrogens Estrogens Signal Transduction Animals Endometriosis Endometriosis Estrogens Female Humans Models, Biological Ovary Ovary Ovary Receptors, Estrogen Receptors, Estrogen

Citation neighborhood

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. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (95)

Cited by (50)

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License: CC0 · commercial use OK