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• W2915590567 endingPage "485" @default.
• W2915590567 startingPage "473" @default.
• W2915590567 abstract "Abstract BACKGROUND Endometriosis is recognized as a steroid-dependent disorder; however, the precise roles of nuclear receptors (NRs) in steroid responsiveness and other signaling pathways are not well understood. OBJECTIVE AND RATIONALE Over the past several years, a number of paradigm-shifting breakthroughs have occurred in the area of NRs in endometriosis. We review and clarify new information regarding the mechanisms responsible for: (i) excessive estrogen biosynthesis, (ii) estrogen-dependent inflammation, (iii) defective differentiation due to progesterone resistance and (iv) enhanced survival due to deficient retinoid production and action in endometriosis. We emphasize the roles of the relevant NRs critical for these pathological processes in endometriosis. SEARCH METHODS We conducted a comprehensive search using PubMed for human, animal and cellular studies published until 2018 in the following areas: endometriosis; the steroid and orphan NRs, estrogen receptors alpha (ESR1) and beta (ESR2), progesterone receptor (PGR), steroidogenic factor-1 (NR5A1) and chicken ovalbumin upstream promoter-transcription factor II (NR2F2); and retinoids. OUTCOMES Four distinct abnormalities in the intracavitary endometrium and extra-uterine endometriotic tissue underlie endometriosis progression: dysregulated differentiation of endometrial mesenchymal cells, abnormal epigenetic marks, inflammation activated by excess estrogen and the development of progesterone resistance. Endometriotic stromal cells compose the bulk of the lesions and demonstrate widespread epigenetic abnormalities. Endometriotic stromal cells also display a wide range of abnormal NR expression. The orphan NRs NR5A1 and NR2F2 compete to regulate steroid-synthesizing genes in endometriotic stromal cells; NR5A1 dominance gives rise to excessive estrogen formation. Endometriotic stromal cells show an abnormally low ESR1:ESR2 ratio due to excessive levels of ESR2, which mediates an estrogen-driven inflammatory process and prostaglandin formation. These cells are also deficient in PGR, leading to progesterone resistance and defective retinoid synthesis. The pattern of NR expression, involving low ESR1 and PGR and high ESR2, is reminiscent of uterine leiomyoma stem cells. This led us to speculate that endometriotic stromal cells may display stem cell characteristics found in other uterine tissues. The biologic consequences of these abnormalities in endometriotic tissue include intense inflammation, defective differentiation and enhanced survival. WIDER IMPLICATIONS Steroid- and other NR-related abnormalities exert genome-wide biologic effects via interaction with defective epigenetic programming and enhance inflammation in endometriotic stromal cells. New synthetic ligands, targeting PGR, retinoic acid receptors and ESR2, may offer novel treatment options." @default.
• W2915590567 created "2019-03-02" @default.
• W2915590567 creator A5009298625 @default.
• W2915590567 creator A5081557771 @default.
• W2915590567 date "2019-02-27" @default.
• W2915590567 modified "2023-10-12" @default.
• W2915590567 title "Endometriosis and nuclear receptors" @default.
• W2915590567 cites W105012709 @default.
• W2915590567 cites W1482806521 @default.
• W2915590567 cites W1483167997 @default.
• W2915590567 cites W1506736207 @default.
• W2915590567 cites W1551972473 @default.
• W2915590567 cites W1569704074 @default.
• W2915590567 cites W1659749843 @default.
• W2915590567 cites W1685873630 @default.
• W2915590567 cites W1825174965 @default.
• W2915590567 cites W1910306760 @default.
• W2915590567 cites W1916521936 @default.
• W2915590567 cites W1964803062 @default.
• W2915590567 cites W1964930501 @default.
• W2915590567 cites W1965260226 @default.
• W2915590567 cites W1967883717 @default.
• W2915590567 cites W1970078194 @default.
• W2915590567 cites W1970572671 @default.
• W2915590567 cites W1971271779 @default.
• W2915590567 cites W1973729104 @default.
• W2915590567 cites W1973817527 @default.
• W2915590567 cites W1974053954 @default.
• W2915590567 cites W1974700967 @default.
• W2915590567 cites W1975412389 @default.
• W2915590567 cites W1976085030 @default.
• W2915590567 cites W1976214975 @default.
• W2915590567 cites W1977873240 @default.
• W2915590567 cites W1978458314 @default.
• W2915590567 cites W1982107116 @default.
• W2915590567 cites W1982512516 @default.
• W2915590567 cites W1984784419 @default.
• W2915590567 cites W1986118680 @default.
• W2915590567 cites W1986411911 @default.
• W2915590567 cites W1987207032 @default.
• W2915590567 cites W1988595534 @default.
• W2915590567 cites W1989252518 @default.
• W2915590567 cites W1993162436 @default.
• W2915590567 cites W1993354065 @default.
• W2915590567 cites W1994567210 @default.
• W2915590567 cites W1998290637 @default.
• W2915590567 cites W1998657660 @default.
• W2915590567 cites W2000299884 @default.
• W2915590567 cites W2002206976 @default.
• W2915590567 cites W2003063828 @default.
• W2915590567 cites W2003363961 @default.
• W2915590567 cites W2009816222 @default.
• W2915590567 cites W2010229505 @default.
• W2915590567 cites W2010311608 @default.
• W2915590567 cites W2012650501 @default.
• W2915590567 cites W2020984639 @default.
• W2915590567 cites W2021918003 @default.
• W2915590567 cites W2021942629 @default.
• W2915590567 cites W2023298070 @default.
• W2915590567 cites W2025995094 @default.
• W2915590567 cites W2026079978 @default.
• W2915590567 cites W2026113746 @default.
• W2915590567 cites W2027569417 @default.
• W2915590567 cites W2027813308 @default.
• W2915590567 cites W2030686715 @default.
• W2915590567 cites W2041320907 @default.
• W2915590567 cites W2044038984 @default.
• W2915590567 cites W2044789514 @default.
• W2915590567 cites W2045114035 @default.
• W2915590567 cites W2045579344 @default.
• W2915590567 cites W2046521626 @default.
• W2915590567 cites W2047249984 @default.
• W2915590567 cites W2047682339 @default.
• W2915590567 cites W2048280620 @default.
• W2915590567 cites W2048412962 @default.
• W2915590567 cites W2049619918 @default.
• W2915590567 cites W2050266242 @default.
• W2915590567 cites W2050276596 @default.
• W2915590567 cites W2050781058 @default.
• W2915590567 cites W2051169220 @default.
• W2915590567 cites W2051981149 @default.
• W2915590567 cites W2052024663 @default.
• W2915590567 cites W2052516455 @default.
• W2915590567 cites W2052734212 @default.
• W2915590567 cites W2052777384 @default.
• W2915590567 cites W2053028196 @default.
• W2915590567 cites W2053265138 @default.
• W2915590567 cites W2053311013 @default.
• W2915590567 cites W2054629971 @default.
• W2915590567 cites W2054715183 @default.
• W2915590567 cites W2054794301 @default.
• W2915590567 cites W2057291577 @default.
• W2915590567 cites W2059605465 @default.
• W2915590567 cites W2064359385 @default.
• W2915590567 cites W2064441872 @default.
• W2915590567 cites W2068018184 @default.
• W2915590567 cites W2069535435 @default.
• W2915590567 cites W2074144170 @default.

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