title: Estrogen biosynthesis and signaling in endometriosis.
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.
authors.affiliation: Department of Physiology, Institute of Biomedicine, University of Turku, 20014 Turku, Finland. kaisa.huhtinen@utu.fi
authors.forename: Kaisa
authors.initials: K
authors.lastname: Huhtinen
authors.forename: Mia
authors.initials: M
authors.lastname: Ståhle
authors.forename: Antti
authors.initials: A
authors.lastname: Perheentupa
authors.forename: Matti
authors.initials: M
authors.lastname: Poutanen
mesh_terms: D000818:Animals; D004715:Endometriosis / Q000378:metabolism* / Q000473:pathology; D004967:Estrogens / Q000096:biosynthesis* / Q000378:metabolism*; D005260:Female; D006801:Humans; D008954:Models, Biological; D010053:Ovary / Q000378:metabolism / Q000473:pathology; D011960:Receptors, Estrogen / Q000378:metabolism; D015398:Signal Transduction
chemical_list: D004967:Estrogens; D011960:Receptors, Estrogen