17β-Hydroxysteroid Dehydrogenase-2 Deficiency and Progesterone Resistance in Endometriosis
Open accessAbstract
Estradiol (E2) stimulates the growth and inflammation in the ectopic endometriotic tissue that commonly resides on the pelvic organs. Several clinical and laboratory-based observations are indicative of resistance to progesterone action in endometriosis. The molecular basis of progesterone resistance in endometriosis may be related to an overall reduction in the levels of progesterone receptor (PR). In normal endometrium, progesterone acts via PR on stromal cells to induce secretion of paracrine factor(s) that in turn stimulate neighboring epithelial cells to express the enzyme 17beta-hydroxysteroid dehydrogenase type 2 (HSD17B2). HSD17B2 is an extremely efficient enzyme and rapidly metabolizes the biologically potent estrogen E2 to weakly estrogenic estrone. In endometriotic tissue, progesterone is incapable of inducing epithelial HSD17B2 expression due to a defect in stromal cells. The inability of endometriotic stromal cells to produce progesterone-induced paracrine factors that stimulate HSD17B2 may be due to the very low levels of PR observed in vivo in endometriotic tissue. The end result is deficient metabolism of E2 in endometriosis giving rise to high local concentrations of this mitogen. The molecular details of this physiological paracrine interaction between the stroma and epithelium in normal endometrium and its lack thereof in endometriosis are discussed.
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- Findingcitation
In endometriotic tissue, progesterone does not induce epithelial HSD17B2 expression.
“In endometriotic tissue, progesterone is incapable of inducing epithelial HSD17B2 expression due to a defect in stromal cells.”
- Also stated in: § Deficient Expression of HSD17B2 in Endometriosis25 · boosted
“We demonstrated that HSD17B2 mRNA and protein are readily detectable in secretory eutopic endometrium but not in paired extraovarian endometriotic samples exposed to the same circulating levels of progesterone.25”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [25]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Also stated in: § Deficient Expression of HSD17B2 in Endometriosis25 · boosted
- Findingcitation
HSD17B2 mRNA and protein are detectable in secretory eutopic endometrium but not in paired extraovarian endometriotic samples exposed to the same progesterone levels.
“We demonstrated that HSD17B2 mRNA and protein are readily detectable in secretory eutopic endometrium but not in paired extraovarian endometriotic samples exposed to the same circulating levels of progesterone.25”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [25]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Findingcitation
In normal endometrium, progesterone acting through stromal progesterone receptors induces paracrine factors that stimulate neighboring epithelial cells to express HSD17B2.
“In normal endometrium, progesterone acts via PR on stromal cells to induce secretion of paracrine factor(s) that in turn stimulate neighboring epithelial cells to express the enzyme 17β-hydroxysteroid dehydrogenase type 2 (HSD17B2).”
- Also stated in: § A Stromal Cell Defect Is Responsible for Deficient HSD17B2 Expression in Endometriotic Tissue · plain
“Physiologically, a stromal PR-mediated paracrine mechanism is responsible for induction of epithelial HSD17B2 expression.”
Quote in the paperSubstantial claim0 of 2 sources checked- cites [18]
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- cites [19]
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- Also stated in: § A Stromal Cell Defect Is Responsible for Deficient HSD17B2 Expression in Endometriotic Tissue · plain
- Findingcitation
Progesterone-induced prolactin mRNA levels in endometriotic cells are much lower than in eutopic endometrial cells.
“Progesterone-induced prolactin mRNA levels in endometriotic cells were much lower compared with eutopic endometrial cells.21”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [21]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Findingcitation
Transcripts of reductive HSD17B1, which catalyzes E1 to E2 conversion, are present in both eutopic endometrium and endometriotic tissue.
“We also demonstrated that transcripts of the reductive HSD17B1, which catalyzes the conversion of E1→E2, were present in both eutopic endometrium and endometriotic tissue.25”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [25]
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- Premisecitation
HSD17B2 enzyme activity and mRNA are present at extremely high levels in eutopic endometrial tissues and epithelial cells from disease-free women during the secretory phase.
“HSD17B2 enzyme activity and mRNA were found to be present in extremely high levels in eutopic endometrial tissues and epithelial cells (from disease-free women) during the secretory phase.12,13,16”
Quote in the paperSubstantial claim0 of 3 sources checked- cites [12]
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- cites [13]
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- cites [16]
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- Interpretationcitation
The failure of progesterone to induce HSD17B2 in endometriotic tissue is caused by a defect in stromal cells.
“In endometriotic tissue, progesterone is incapable of inducing epithelial HSD17B2 expression due to a defect in stromal cells.”
- Also stated in: § A Stromal Cell Defect Is Responsible for Deficient HSD17B2 Expression in Endometriotic Tissue · hedged
“Taken together, a stromal cell defect in endometriosis appears to be responsible for the lack of progesterone-mediated secretion of factors that induce Sp1 production and its binding activity to the HSD17B2 promoter for expression of this gene in epithelial cells.30”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [30]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Also stated in: § A Stromal Cell Defect Is Responsible for Deficient HSD17B2 Expression in Endometriotic Tissue · hedged
- Premisecitation
HSD17B2 rapidly metabolizes the potent estrogen E2 to weakly estrogenic estrone.
“HSD17B2 is an extremely efficient enzyme and rapidly metabolizes the biologically potent estrogen E2 to weakly estrogenic estrone.”
- Also stated in: § PARACRINE GENE REGULATION BY PROGESTERONE RECEPTOR IN ENDOMETRIUM · plain
“The antiestrogenic effect of progesterone in endometrial tissue is in part mediated by its stimulation of 17β-hydroxysteroid dehydrogenase type 2 activity, which catalyzes the conversion of biologically active E2 to the inactive steroid estrone (E1).12–14”
Quote in the paperSubstantial claim0 of 3 sources checked- cites [12]
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- cites [13]
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- cites [14]
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- Also stated in: § PARACRINE GENE REGULATION BY PROGESTERONE RECEPTOR IN ENDOMETRIUM · plain
- Premisecitation
Progesterone did not induce conversion of E2 to E1 in endometriotic tissue, unlike in eutopic endometrium.
“It was previously reported that progesterone did not induce the conversion of E2→E1 in endometriotic tissue, in contrast to eutopic endometrium.26”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [26]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Interpretationreasoning
Deficient metabolism of E2 in endometriosis leads to high local concentrations of E2.
“The end result is deficient metabolism of E2 in endometriosis giving rise to high local concentrations of this mitogen.”
- Also stated in: § Deficient Expression of HSD17B2 in Endometriosis25 · plain
“Local concentrations of E2 in endometriotic tissues are further amplified by the lack of HSD17B2 expression and subsequent metabolism of E2→E1.”
Quote in the paperSubstantial claim - Also stated in: § Deficient Expression of HSD17B2 in Endometriosis25 · plain
- Interpretationown data
The absence of PR-B protein in endometriotic tissue is related to transcription.
“These data suggest that the absence of PR-B protein in endometriotic tissue is transcription related (our unpublished observations).”
Quote in the paperSubstantial claim - Interpretationreasoning
The inability of endometriotic stromal cells to produce progesterone-induced paracrine factors that stimulate HSD17B2 may be due to very low progesterone receptor levels in vivo in endometriotic tissue.
“The inability of endometriotic stromal cells to produce progesterone-induced paracrine factors that stimulate HSD17B2 may be due to the very low levels of PR observed in vivo in endometriotic tissue.”
Quote in the paperSubstantial claim - Interpretationreasoning
Multiple molecular mechanisms contribute to increased estrogenic activity in endometriosis compared with eutopic endometrial tissue.
“Taken together, multiple molecular mechanisms contribute to the increased estrogenic activity in endometriosis as compared with eutopic endometrial tissue.”
Quote in the paperSubstantial claim - Interpretationreasoning
Deficient progesterone action is localized to a stromal cell defect in endometriosis.
“We localized deficient progesterone action to a stromal cell defect in endometriosis.”
Quote in the paperSubstantial claim - Interpretationcitation
These findings support impaired stromal differentiation due to relative resistance to progesterone action in endometriosis.
“These findings further support the concept of impaired stromal differentiation owing to a relative resistance to progesterone action in endometriosis.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [21]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Interpretationreasoning
The weakly estrogenic E1 is readily converted to potent E2 in endometriotic tissues.
“Thus the weakly estrogenic product of the aromatase reaction, E1, is readily converted to the potent estrogen, E2, in endometriotic tissues.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [25]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Interpretationnone given
Progesterone resistance in endometriosis is primarily due to significantly lower PR-B and total progesterone receptor levels in endometriotic stromal cells compared with endometrial stromal cells.
“It is likely that progesterone resistance is primarily due to significantly lower PR-B and total PR in endometriotic stromal cells compared with endometrial stromal cells.”
Quote in the paperNot a substantial claim - Interpretationcitation
A stromal cell defect in endometriosis is responsible for the lack of progesterone-mediated secretion of factors that induce Sp1 production and its binding to the HSD17B2 promoter for epithelial expression.
“Taken together, a stromal cell defect in endometriosis appears to be responsible for the lack of progesterone-mediated secretion of factors that induce Sp1 production and its binding activity to the HSD17B2 promoter for expression of this gene in epithelial cells.30”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [30]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Interpretationown data
The lack of HSD17B2 in endometriotic epithelial cells despite histologically detectable secretory changes suggests selective resistance to certain progesterone actions.
“The lack of HSD17B2 in endometriotic epithelial cells of matched tissues despite histologically detectable secretory changes in response to progesterone suggested that endometriotic tissue exhibits selective resistance to certain actions of progesterone.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [25]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- May combine two claims. 7
May combine two claims.
FindingcitationIn eutopic endometrium, PR-B protein and mRNA levels increase during the proliferative phase, peak before ovulation, and diminish after ovulation, suggesting that E2 stimulates PR-B.
“In eutopic endometrium, PR-B protein and mRNA levels progressively increased during the proliferative phase, peaked immediately before ovulation, and diminished after ovulation, suggesting that E2 stimulates PR-B levels.9”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [9]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
May combine two claims.
Findingown dataProgesterone receptor-B and total progesterone receptor levels are significantly decreased in endometriotic tissues and cells compared with eutopic endometrium.
“Previous immunohistochemical studies revealed that PR levels are lower in endometriotic tissue compared with eutopic endometrium.22–24”
- Also stated in: § Progesterone Receptor-B and Total Progesterone Receptors Are Significantly Decreased in Endometriotic Tissues and Cells9 · plain
“In a separate matched tissue set of eutopic endometrial samples and ovarian endometrioma cyst walls, Affymetrix gene microarray (confirmed by real-time polymerase chain reaction [PCR]) showed severely decreased PR-B (11-fold) and total PR (8-fold) mRNA levels.”
Quote in the paperSubstantial claim0 of 4 sources checked- cites [9]
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- cites [22]
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- cites [23]
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- cites [24]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Also stated in: § Progesterone Receptor-B and Total Progesterone Receptors Are Significantly Decreased in Endometriotic Tissues and Cells9 · plain
May combine two claims.
FindingcitationConditioned medium from progestin-pretreated endometrial stromal cells stimulates Sp1 protein and HSD17B2 mRNA and promoter activity in endometrial epithelial cells, whereas conditioned medium from endometriotic stromal cells fails to induce Sp1 or HSD17B2.
“The addition of conditioned medium from progestin-pretreated endometrial stromal cells significantly stimulated Sp1 protein and HSD17B2 mRNA and promoter activity in endometrial epithelial cells.30”
- Also stated in: § A Stromal Cell Defect Is Responsible for Deficient HSD17B2 Expression in Endometriotic Tissue · plain
“In contrast, conditioned medium from endometriotic stromal cells failed to induce Sp1 or HSD17B2 in epithelial cells (Fig. 3).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [30]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Also stated in: § A Stromal Cell Defect Is Responsible for Deficient HSD17B2 Expression in Endometriotic Tissue · plain
May combine two claims.
InterpretationcitationProgesterone resistance in endometriotic tissue may be due to an overall reduction in progesterone receptors and the absence of PR-B.
“Thus progesterone resistance in endometriotic tissue may be due to an overall reduction in PR and the absence of PR-B.9”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [9]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
May combine two claims.
Interpretationown dataE2 inactivation is impaired in endometriotic tissues because HSD17B2 expression is deficient, whereas HSD17B2 is normally expressed in eutopic endometrium in response to progesterone.
“We also observed that inactivation of E2 is impaired in endometriotic tissues due to deficient expression of HSD17B2, which is normally expressed in eutopic endometrium in response to progesterone.25”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [25]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
May combine two claims.
InterpretationreasoningProgesterone receptor deficiency is likely responsible for increased E2 levels in endometriosis because progesterone fails to induce HSD17B2 in endometriotic tissue.
“PR deficiency is likely responsible for increased levels of E2 in endometriosis because progesterone fails to induce the E2-metabolizing enzyme HSD17B2 in endometriotic tissue (Fig. 3).”
Quote in the paperSubstantial claimMay combine two claims.
PremisecitationAberrant aromatase expression in endometriotic stromal cells favors conversion of androstenedione to E1, whereas aromatase is normally absent in eutopic endometrium.
“Furthermore, aberrant aromatase expression in endometriotic stromal cells favors the conversion of androstenedione to E1; aromatase expression is normally absent in the eutopic endometrium.29”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [29]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
The paper relies on this without support.
E2 stimulates growth and inflammation in ectopic endometriotic tissue that commonly resides on pelvic organs.
“Estradiol (E2) stimulates the growth and inflammation in the ectopic endometriotic tissue that commonly resides on the pelvic organs.”
The paper relies on this without support.
Clinical and laboratory observations indicate resistance to progesterone action in endometriosis.
“Several clinical and laboratory-based observations are indicative of resistance to progesterone action in endometriosis.”
The paper relies on this without support.
Progesterone induces differentiation of endometrial stromal and epithelial cells.
“Progesterone induces the differentiation of both endometrial stromal and epithelial cells as exemplified by decidual and secretory changes and reduction in epithelial cell proliferation.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Local estrogen production and progesterone resistance were demonstrated in larger endometriosis lesions.
“Local estrogen production (154) and progesterone resistance (155-162) were demonstrated in larger endometriosis lesions (154-163)”
From Pathogenesis of endometriosis: The genetic/epigenetic theory (2019) · cites this paper as [158]
In endometriotic lesions, stromal cells showing progesterone resistance are unable to produce retinoic acid, resulting in loss of 17β-HSD2 expression, failure to inactivate local E2, and high E2 activity.
“Conversely, in endometriotic lesions, stromal cells showing progesterone resistance are unable to produce RA which results in loss of 17β-HSD2 expression and failure to inactivate local E2, ultimately leading to high E2 activity [14,15,16,20,21,22].”
From Endometriosis and Medical Therapy: From Progestogens to Progesterone Resistance to GnRH Antagonists: A Review (2021) · cites this paper as [14]
In endometrial stromal cells, progesterone increases formation of retinoic acid, which triggers expression of 17β-HSD2 in epithelial cells.
“In endometrial stromal cells, progesterone increases formation of RA, which triggers expression of 17β-HSD2 in epithelial cells.”
From Endometriosis and Medical Therapy: From Progestogens to Progesterone Resistance to GnRH Antagonists: A Review (2021) · cites this paper as [14]
During the luteal phase, progesterone acts through PR-B and boosts transcription and secretion of 17β-HSD2, which converts E2 to less active estrone.
“During the luteal phase, progesterone acts through PR-B and boosts transcription and secretion of 17β-hydroxysteroid dehydrogenase type 2 (17β-HSD2), responsible for converting E2 to the less active estrone [14,15,16].”
From Endometriosis and Medical Therapy: From Progestogens to Progesterone Resistance to GnRH Antagonists: A Review (2021) · cites this paper as [14]
During the follicular phase, estrogen acts on eutopic endometrium through ER to increase transcription and protein levels of PR, especially PR-B.
“During the follicular phase, estrogen acts on eutopic endometrium through the estrogen receptor (ER) to increase transcription and protein levels of the progesterone receptor (PR), especially the PR-B isoform.”
From Endometriosis and Medical Therapy: From Progestogens to Progesterone Resistance to GnRH Antagonists: A Review (2021) · cites this paper as [14]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
PR-B is described as both present and undetectable in eutopic endometrium
MinorThe paper first reports measurable PR-B protein and mRNA in eutopic endometrium across the menstrual cycle, then says neither was detectable in any matched extraovarian eutopic endometrial samples. The latter statement conflicts with the reported expression pattern and appears to identify the wrong tissue.
“In contrast, PR-B mRNA and protein levels were not detectable in any of the matched extraovarian eutopic endometrial samples (Fig. 1).”
“In eutopic endometrium, PR-B protein and mRNA levels progressively increased during the proliferative phase, peaked immediately before ovulation, and diminished after ovulation, suggesting that E2 stimulates PR-B levels.9”
Cites
Kastner, P., Krust, A., Turcotte, B., Stropp, U., Tora, L., Gronemeyer, H., & Chambon, P. (1990) · The EMBO Journal · doi:10.1002/j.1460-2075.1990.tb08280.x · Cited by 1,534 · see citing works
Burney, R. O., Talbi, S., Hamilton, A. E., Vo, K. C., Nyegaard, M., Nezhat, C. R., Lessey, B. A., & Giudice, L. C. (2007) · Endocrinology · doi:10.1210/en.2006-1692 · Cited by 735 · cited 1× · see citing works
“Our conclusion resonates with gene expression microarray studies performed on eutopic endometrium of women with endometriosis compared with that from disease-free women.(31,32) These studies on eutopic endometrium identified distinct molecular defects that are consistent with the progesterone resistance hypothesis.”
ResultSubgroup of reproductive functions of progesterone mediated by progesterone receptor-B isoform
Mulac-Jericevic, B., Mullinax, R. A., DeMayo, F. J., Lydon, J. P., & Conneely, O. M. (2000) · Science · doi:10.1126/science.289.5485.1751 · Cited by 704 · cited 1× · see citing works
“PR-A is both necessary and sufficient to elicit the progesterone-dependent uterine and ovarian responses necessary for female fertility, whereas the PR-B isoform is required to elicit normal responses of the mammary gland to progesterone.(7) In human endometrial tissue, PR-B is likely to play a more important biologic…”
BackgroundKao, L. C., Germeyer, A., Tulac, S., Lobo, S., Yang, J. P., Taylor, R. N., Osteen, K., Lessey, B. A., & Giudice, L. C. (2003) · Endocrinology · doi:10.1210/en.2003-0043 · Cited by 696 · cited 1× · see citing works
“Our conclusion resonates with gene expression microarray studies performed on eutopic endometrium of women with endometriosis compared with that from disease-free women.(31,32) These studies on eutopic endometrium identified distinct molecular defects that are consistent with the progesterone resistance hypothesis.”
ResultProgesterone Receptor Isoform A But Not B Is Expressed in Endometriosis
Attia, G. R. (2000) · Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.85.8.2897 · Cited by 488 · see citing works
Wu, L., Einstein, M., Geissler, W. M., Chan, H. K., Elliston, K. O., & Andersson, S. (1993) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(18)31480-7 · Cited by 437 · see citing works
Progesterone resistance in endometriosis: link to failure to metabolize estradiol.
Bulun, S. E., Cheng, Y.-H., Yin, P., Imir, G., Utsunomiya, H., Attar, E., Innes, J., & Julie Kim, J. (2006) · Molecular and Cellular Endocrinology · doi:10.1016/j.mce.2005.11.041 · Cited by 397 · cited 2× · see citing works
“Progesterone-induced prolactin mRNA levels in endometriotic cells were much lower compared with eutopic endometrial cells.(21) These findings further support the concept of impaired stromal differentiation owing to a relative resistance to progesterone action in endometriosis.”
BackgroundResultSelf-citationGiangrande, P. H., & McDonnell, D. P. (1999) · PubMed · Cited by 339 · see citing works
Zeitoun, K., Takayama, K., Sasano, H., Suzuki, T., Moghrabi, N., Andersson, S., Johns, A., Meng, L., Putman, M., Carr, B., et al. (1998) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem.83.12.5301 · Cited by 308 · see citing works
Self-citationInduction of Human Endometrial Estradiol Dehydrogenase by Progestins
Tseng, L., & Gurpide, E. (1975) · Endocrinology · doi:10.1210/endo-97-4-825 · Cited by 301 · cited 5× · see citing works
“HSD17B2 enzyme activity and mRNA were found to be present in extremely high levels in eutopic endometrial tissues and epithelial cells (from disease-free women) during the secretory phase.(12,13,16) We demonstrated that HSD17B2 mRNA and protein are readily detectable in secretory eutopic endometrium but not in paired…”
BackgroundInfluentialMote, P. A., Balleine, R. L., McGowan, E. M., & Clarke, C. L. (1999) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem.84.8.5928 · Cited by 270 · see citing works
Molecular Cloning of the Chicken Progesterone Receptor
Conneely, O. M., Sullivan, W. P., Toft, D. O., Birnbaumer, M., Cook, R. G., Maxwell, B. L., Zarucki-Schulz, T., Greene, G. L., Schrader, W. T., & O’Malley, B. W. (1986) · Science · doi:10.1126/science.2426779 · Cited by 242 · see citing works
Horwitz, K. B., & Alexander, P. (1983) · Endocrinology · doi:10.1210/endo-113-6-2195 · Cited by 235 · see citing works
Progestins for symptomatic endometriosis: a critical analysis of the evidence
Vercellini, P., Cortesi, I., & Crosignani, P. G. (1997) · Fertility and Sterility · doi:10.1016/s0015-0282(97)00193-3 · Cited by 229 · cited 1× · see citing works
“Furthermore, aberrant aromatase expression in endometriotic stromal cells favors the conversion of androstenedione to E1; aromatase expression is normally absent in the eutopic endometrium.(29) We also demonstrated that transcripts of the reductive HSD17B1, which catalyzes the conversion of E1!E2, were present in both…”
BackgroundCasey, M. L., MacDonald, P. C., & Andersson, S. (1994) · Journal of Clinical Investigation · doi:10.1172/jci117569 · Cited by 212 · see citing works
Tseng, L., & Gurpide, E. (1974) · Endocrinology · doi:10.1210/endo-94-2-419 · Cited by 175 · see citing works
Kurita, T., Lee, K.-J., Cooke, P. S., Lydon, J. P., & Cunha, G. R. (2000) · Biology of Reproduction · doi:10.1095/biolreprod62.4.831 · Cited by 150 · see citing works
Self-citationLESSEY, B. A., SUE ALEXANDER, P., & HORWITZ, K. B. (1983) · Endocrinology · doi:10.1210/endo-112-4-1267 · Cited by 141 · see citing works
Differential expression of uterine progesterone receptor forms A and B during the menstrual cycle
Mangal, R. K., Wiehle, R. D., Poindexter, A. N., & Weigel, N. L. (1997) · The Journal of Steroid Biochemistry and Molecular Biology · doi:10.1016/s0960-0760(97)00119-2 · Cited by 132 · cited 1× · see citing works
“In human endometrial tissue, PR-B is likely to play a more important biological role in the endometrium because PR-B, but not PR-A, levels are tightly regulated by estradiol (E2) during the human menstrual cycle.(8,9) The in vivo distribution of PR-A and PR-B in the endometrium was reported to be cell and cycle specif…”
BackgroundAlexander, I. E., Clarke, C. L., Shine, J., & Sutherland, R. L. (1989) · Molecular Endocrinology · doi:10.1210/mend-3-9-1377 · Cited by 109 · see citing works
Vierikko, P., Kauppila, A., Rönnberg, L., & Vihko, R. (1985) · Fertility and Sterility · doi:10.1016/s0015-0282(16)48376-7 · Cited by 99 · see citing works
Prentice, A., Randall, B., Weddell, A., McGill, A. C., Henry, L., Horne, C. H. W., & Thomas, E. J. (1992) · Human Reproduction · doi:10.1093/oxfordjournals.humrep.a137848 · Cited by 91 · see citing works
Bergqvist, A., & Fernö, M. (1993) · Human Reproduction · doi:10.1093/oxfordjournals.humrep.a138005 · Cited by 86 · see citing works
Yang, S., Fang, Z., Gürateş, B., Tamura, M., Miller, J., Ferrer, K., & Bulun, S. E. (2001) · Molecular Endocrinology · doi:10.1210/mend.15.12.0742 · Cited by 86 · see citing works
Self-citationMustonen, M. V. J., Isomaa, V. V., Vaskivuo, T., Tapanainen, J., Poutanen, M. H., Stenbäck, F., Vihko, R. K., & Vihko, P. T. (1998) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem.83.4.4709 · Cited by 84 · see citing works
Cheng, Y.-H., Yin, P., Xue, Q., Yilmaz, B., Dawson, M. I., & Bulun, S. E. (2008) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2007-1536 · Cited by 71 · see citing works
Self-citationSATYASWAROOP, P. G., WARTELL, D. J., & Mortel, R. (1982) · Endocrinology · doi:10.1210/endo-111-3-743 · Cited by 66 · see citing works
Cheng, Y.-H., Imir, A. G., Fenkçi, V., Yılmaz, M. B., & Bulun, S. E. (2007) · American Journal of Obstetrics and Gynecology · doi:10.1016/j.ajog.2006.12.014 · Cited by 56 · cited 3× · see citing works
“Taken together, a stromal cell defect in endometriosis appears to be responsible for the lack of progesterone-mediated secretion of factors that induce Sp1 production and its binding activity to the HSD17B2 promoter for expression of this gene in epithelial cells.(30) This may be a key molecular consequence clinically…”
BackgroundInfluentialSelf-citationBergqvist, A., & Fernö, M. (1993) · Fertility and Sterility · doi:10.1016/s0015-0282(16)56037-3 · Cited by 52 · see citing works
Cheng, Y.-H., Imir, A. G., Suzuki, T., Fenkçi, V., Yılmaz, B., Sasano, H., & Bulun, S. E. (2006) · Biology of Reproduction · doi:10.1095/biolreprod.106.051912 · Cited by 44 · see citing works
Self-citationSteroid Biosynthetic Enzymes: 17 β Hydroxysteroid Dehydrogenase
ISOMAA, V. V., Ghersevich, S. A., Mäentausta, O., Peltoketo, H., POUTANEN, M. H., & Vihko, R. (1993) · Annals of Medicine · doi:10.3109/07853899309147864 · Cited by 22 · see citing works
Labrie, F., Luu-The, V., Labrie, C., Bérubé, D., Couët, J., Zhao, H., Gagné, R., & Simard, J. (1989) · Journal of Steroid Biochemistry · doi:10.1016/0022-4731(89)90082-4 · Cited by 20 · see citing works
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Pathogenesis of endometriosis: The genetic/epigenetic theory
Koninckx, P. R., Ussia, A., Adamyan, L., Wattiez, A., Gomel, V., & Martin, D. C. (2019) · Fertility and Sterility · doi:10.1016/j.fertnstert.2018.10.013 · Cited by 427 · see citing works
Pathogenesis of deep endometriosis
Gordts, S., Koninckx, P., & Brosens, I. (2017) · Fertility and Sterility · doi:10.1016/j.fertnstert.2017.08.036 · Cited by 241 · see citing works
Endometriosis and adenomyosis: shared pathophysiology
Bulun, S. E., Yildiz, S., Adli, M., Chakravarti, D., Parker, J. B., Milad, M., Yang, L., Chaudhari, A., Tsai, S., Wei, J. J., et al. (2023) · Fertility and Sterility · doi:10.1016/j.fertnstert.2023.03.006 · Cited by 216 · see citing works
Self-citationCasper, R. F. (2017) · Fertility and Sterility · doi:10.1016/j.fertnstert.2017.01.003 · Cited by 205 · see citing works
“In endometriotic implants, ER-a is reduced but ER-b activity is markedly upregulated (15, 16), leading to complete loss of PR-B (17) and the inability to induce HSD17B2 (12).”
BackgroundPeter, A. W., Adamson, G. D., Al‐Jefout, M., Becker, C. M., D’Hooghe, T. M., Dunselman, G. A. J., Fazleabas, A. T., Giudice, L. C., Horne, A. W., Hull, M. L., et al. (2016) · Reproductive Sciences · doi:10.1177/1933719116654991 · Cited by 188 · see citing works
Donnez, J., & Dolmans, M.-M. (2021) · Journal of Clinical Medicine · doi:10.3390/jcm10051085 · Cited by 182 · see citing works
A new concept of endometriosis and adenomyosis, tissue injury and repair (TIAR)
Leyendecker, G., & Wildt, L. (2011) · hmbci · doi:10.1515/hmbci.2011.002 · Cited by 147 · see citing works
Aromatase inhibitors for the treatment of endometriosis
Pavone, M. E., & Bulun, S. E. (2012) · Fertility and Sterility · doi:10.1016/j.fertnstert.2012.08.053 · Cited by 138 · see citing works
Self-citationLoss of HDAC3 results in nonreceptive endometrium and female infertility
Kim, T. H., Yoo, J., Choi, K., Shin, J., Leach, R. E., Fazleabas, A. T., Young, S. L., Lessey, B. A., Yoon, H., & Jeong, J. (2019) · Science Translational Medicine · doi:10.1126/scitranslmed.aaf7533 · Cited by 142 · see citing works
Uterine biology in pigs and sheep
Bazer, F. W., Song, G., Kim, J. Y., Dunlap, K. A., Satterfield, M. C., Johnson, G. A., Burghardt, R. C., & Wu, G. (2012) · Journal of Animal Science and Biotechnology/Journal of animal science and biotechnology · doi:10.1186/2049-1891-3-23 · Cited by 142 · see citing works
“, fibroblast growth factors-7 (FGF7) and −10 (FGF10) and hepatocyte growth factor (HGF) in sheep uteri [50] or FGF7, HGF and retinoic acid in primates [44,51].”
BackgroundHan, S. J., & O’Malley, B. W. (2014) · Human Reproduction Update · doi:10.1093/humupd/dmu002 · Cited by 98 · see citing works
“…endometriotic tissues from locally elevated levels of aromatase along with reduced activity of 17b-hydroxysteroid dehydrogenase-2 (Brosens et al.; Bulun et al., 2010a, b), current endometriosis treatments also involve suppressing E2 levels through the use of GnRH agonists (Descamps and Lansac,…”
BackgroundHDAC1 and HDAC2 are Differentially Expressed in Endometriosis
Colón-Díaz, M., Báez, P., García, M., Ruiz, A., Monteiro, J. B., Fourquet, J., Bayona, M., Alvarez-Garriga, C., Achille, A., Seto, E., et al. (2012) · Reproductive Sciences · doi:10.1177/1933719111432870 · Cited by 88 · see citing works
“is lost leading to increased levels in endometriosis.(29) This, in turn, would result in a hypoacetylated state and aberrant gene expression profiles.”
BackgroundPolyphenols as a Diet Therapy Concept for Endometriosis—Current Opinion and Future Perspectives
Gołąbek-Grenda, A., Kowalska, K., & Olejnik, A. M. (2021) · Nutrients · doi:10.3390/nu13041347 · Cited by 93 · see citing works
van der Horst, P. H., Wang, Y., van der Zee, M., Burger, C. W., & Blok, L. J. (2011) · Molecular and Cellular Endocrinology · doi:10.1016/j.mce.2011.06.010 · Cited by 80 · see citing works
Altered retinoid uptake and action contributes to cell survival in endometriosis
Pavone, M. E., Reierstad, S., Sun, H., Milad, M., Bulun, S. E., & Cheng, Y.-H. (2010) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2010-0459 · Cited by 74 · see citing works
Self-citationEndometriosis: a life cycle approach?
Brosens, I., Puttemans, P., & Benagiano, G. (2013) · American Journal of Obstetrics and Gynecology · doi:10.1016/j.ajog.2013.03.009 · Cited by 66 · see citing works
In vitro and in vivo ocular biocompatibility of electrospun poly(ɛ-caprolactone) nanofibers
da Silva, G. R., de Lima, T. H., Oréfice, R. L., et al. (2015) · European Journal of Pharmaceutical Sciences · doi:10.1016/j.ejps.2015.03.003 · Cited by 58 · see citing works
Pavone, M. E., Dyson, M., Reirstad, S., Pearson, E., Ishikawa, H., Cheng, Y. H., & Bulun, S. E. (2011) · Human Reproduction · doi:10.1093/humrep/der172 · Cited by 56 · see citing works
“factors mediating the progesterone-dependent induction of HSD17B2, and we hypothesize that defective retinoid metabolism in endometriotic stromal cells contributes to reduced E2 metabolism and increased cell survival in endometriosis (Nobel et al., 1997; Bulun et al., 2006; Cheng et al., 2006, 2007; Bulun, 2009; Bulun…”
BackgroundSelf-citationStructure, Function, and Evaluation of the Female Reproductive Tract
Lessey, B. A., & Young, S. L. (2019) · Elsevier eBooks · doi:10.1016/b978-0-323-47912-7.00009-3 · Cited by 58 · see citing works
Logan, P. C., Yango, P., & Tran, N. D. (2017) · Reproductive Sciences · doi:10.1177/1933719117704905 · Cited by 54 · see citing works
“Progesterone resistance is also due to aberrant expression of steroid biosynthesis enzymes in endometriotic stromal and epithelial cells.(63,105) The aldo-keto reductases AKR1C1/2/3 are progesterone and steroid metabolizers that are upregulated in endometriosis.”
BackgroundEndometriosis, infertility and MicroRNA’s: A review
Raja, M. H. R., Farooqui, N., Zuberi, N., Ashraf, M., Azhar, A., Baig, R., Badar, B., & Rehman, R. (2021) · Journal of Gynecology Obstetrics and Human Reproduction · doi:10.1016/j.jogoh.2021.102157 · Cited by 53 · see citing works
Bentamapimod (JNK Inhibitor AS602801) Induces Regression of Endometriotic Lesions in Animal Models
Palmer, S. S., Altan, M., Denis, D., Tos, E. G., Gotteland, J., Osteen, K. G., Bruner‐Tran, K. L., & Nataraja, S. G. (2015) · Reproductive Sciences · doi:10.1177/1933719115600553 · Cited by 54 · see citing works
“In endometriotic tissue, PR is incapable of inducing epithelial HSD17B2 expression due to the very low levels of PR in endometriotic tissue.(43) In the present study, gene expression analysis of the endometriotic lesions following bentamapimod treatment showed no change in the expression of PR and ER, although express…”
BackgroundLaganà, A. S., Sturlese, E., Retto, G., Sofo, V., & Triolo, O. (2013) · Obstetrics and Gynecology International · doi:10.1155/2013/527041 · Cited by 51 · see citing works
Donnez, J., & Dolmans, M. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms222111342 · Cited by 49 · see citing works
Hevir, N., Vouk, K., Šinkovec, J., Ribič-Pucelj, M., & Lanišnik Rižner, T. (2011) · Chemico-Biological Interactions · doi:10.1016/j.cbi.2011.01.003 · Cited by 48 · see citing works
“Disturbed progesterone action in endometriosis is usually explained by decreased levels of the progesterone receptors, PR-A and B (PRAB), or a lack of PR-B expression [8,9], while little is known about the pre-receptor metabolism of progesterone [10].”
BackgroundPotential role of aromatase inhibitors in the treatment of endometriosis
Hashim, H. A. (2014) · International Journal of Women s Health · doi:10.2147/ijwh.s34684 · Cited by 46 · see citing works
“This has been attributed to a defective function of stromal cells of endometriosis, resulting in failure to induce the expression of the epithelial 17β-hydroxysteroid dehydrogenase type 2 enzyme (17β-HSD2) responsible for the conversion of E 2 to estrone.(5,15,16)”
Inhibition of steroid sulfatase decreases endometriosis in an in vivo murine model
Colette, S., Defrere, S., Lousse, J. C., Van Langendonckt, A., Gotteland, J. P., Loumaye, E., & Donnez, J. (2011) · Human Reproduction · doi:10.1093/humrep/der079 · Cited by 45 · see citing works
“estrone (Bulun et al., 2010).”
BackgroundSamartzis, N., Samartzis, E. P., Noske, A., Fedier, A., Dedes, K. J., Caduff, R., Fink, D., & Imesch, P. (2012) · Reproductive Biology and Endocrinology · doi:10.1186/1477-7827-10-30 · Cited by 43 · see citing works
“The classic estrogen signaling pathway is thought to be mediated by two nuclear estrogen receptors (ER-alpha and ER-beta), which are encoded by different genes [11,17].”
BackgroundKipp, M., Berger, K., Clarner, T., Dang, J., & Beyer, C. (2012) · Journal of neuroendocrinology · doi:10.1111/j.1365-2826.2011.02163.x · Cited by 41 · see citing works
Bufalin suppresses endometriosis progression by inducing pyroptosis and apoptosis
Cho, Y. J., Lee, J. E., Park, M. J., O’Malley, B. W., & Han, S. J. (2018) · Journal of Endocrinology · doi:10.1530/joe-17-0700 · Cited by 37 · see citing works
Activated glucocorticoid and eicosanoid pathways in endometriosis
Monsivais, D., Bray, J. D., Su, E. J., Pavone, M. E., Dyson, M. T., Navarro, A., Kakinuma, T., & Bulun, S. E. (2012) · Fertility and Sterility · doi:10.1016/j.fertnstert.2012.03.030 · Cited by 37 · see citing works
Self-citationEmerging Drug Targets for Endometriosis
Dolmans, M., & Donnez, J. (2022) · Biomolecules · doi:10.3390/biom12111654 · Cited by 38 · see citing works
Park, Y., Cho, Y. J., Sung, N., Park, M. J., Guan, X., Gibbons, W. E., O’Malley, B. W., & Han, S. J. (2022) · Journal of Biomedical Science · doi:10.1186/s12929-022-00883-2 · Cited by 32 · see citing works
Zhou, Y., Jorgensen, E. M., Gan, Y., & Taylor, H. S. (2011) · Biology of Reproduction · doi:10.1095/biolreprod.110.087494 · Cited by 28 · see citing works
90 YEARS OF PROGESTERONE: Selective progesterone receptor modulators in gynaecological therapies
Critchley, H., & Chodankar, R. R. (2020) · Journal of Molecular Endocrinology · doi:10.1530/jme-19-0238 · Cited by 25 · see citing works
Sohler, F., Sommer, A., Wachter, D. L., Agaimy, A., Fischer, O. M., Renner, S. P., Burghaus, S., Fasching, P. A., Beckmann, M. W., Fuhrmann, U., et al. (2012) · Reproductive Sciences · doi:10.1177/1933719112451147 · Cited by 25 · see citing works
“Decreased PGR expression, especially the loss of the PGR-B isoform but not PGR-A, has been implicated as one cause for lower HSD17B2 expression and a P4 resistance phenotype in endometriosis lesions related to therapy.(54,55) However, it is unknown at present how PGR-A target gene regulation is affected in endometriot…”
BackgroundNazmeen, A., Chen, G., Ghosh, T. K., & Maiti, S. (2020) · Cancer Cell International · doi:10.1186/s12935-020-1153-y · Cited by 20 · see citing works
“E1 subsequently converted to estradiol (E2) by 17β-HSD type 1 [42] affecting breast cancer cells through ERα and ERβ.”
BackgroundPašková, A., Pařı́zek, A., Hill, M., Velíková, M., Kubátová, J., Dušková, M., Adamcová, K., Koucký, M., Šimják, P., ČERNÝ, A., et al. (2014) · Physiological Research · doi:10.33549/physiolres.932624 · Cited by 23 · see citing works
“…1994), there is growing evidence that multicomponent analyses of steroids in umbilical cord blood at labor may be also effective for predicting endocrine diseases during the subsequent life of the newborn (Baik et al. 2005, Bulun et al. 2010, Jari et al. 2004, Troisi et al. 2008, Yang et al. 2007).”
BackgroundDonnez, J., Cacciottola, L., Squifflet, J.-L., & Dolmans, M. (2023) · Drug Design Development and Therapy · doi:10.2147/dddt.s269976 · Cited by 22 · see citing works
Arosh, J. A., Lee, J., & Banu, S. K. (2021) · Molecular and Cellular Endocrinology · doi:10.1016/j.mce.2021.111446 · Cited by 17 · see citing works
Bressler, L. H. (2017) · doi:10.24966/rmgo-2574/100008 · Cited by 17 · see citing works
“Aberrant proliferation and survival of endometriotic tissue has been associated with progesterone resistance whereby endometriotic tissue does not display the typical antiproliferative and differentiative response to progesterone [1,2].”
Amanda, C. R., Asmarinah, A., Hestiantoro, A., Tulandi, T., & Febriyeni (2024) · European Journal of Obstetrics & Gynecology and Reproductive Biology · doi:10.1016/j.ejogrb.2024.07.061 · Cited by 14 · see citing works
Poirier, D., Nyachieo, A., Romano, A., Roy, J., Maltais, R., Chai, D. C., Delvoux, B., Tomassetti, C., & Vanhie, A. (2022) · The Journal of Steroid Biochemistry and Molecular Biology · doi:10.1016/j.jsbmb.2022.106136 · Cited by 14 · see citing works
Zipponi, M., Cacciottola, L., & Dolmans, M. (2024) · Human Reproduction · doi:10.1093/humrep/deae116 · Cited by 14 · see citing works
Role of adipokines in embryo implantation
Jafari-Gharabaghlou, D., Vaghari-Tabari, M., Oghbaei, H., Lotz, L., Zarezadeh, R., Rezaei, Y. R., Ranjkesh, M., Nouri, M., Fattahi, A., Nikanfar, S., et al. (2021) · Endocrine Connections · doi:10.1530/ec-21-0288 · Cited by 10 · see citing works
Endometrial stromal cell attachment and matrix homeostasis in abdominal wall endometriomas
Itoh, H., Mogami, H., Nemer, L. B., et al. (2017) · Human Reproduction · doi:10.1093/humrep/dex371 · Cited by 14 · see citing works
Kulmány, Á. E., Herman, B. E., Zupkó, I., Sinreih, M., Rižner, T. L., Savić, M. P., Oklješa, A. M., Nikolić, A. R., Nagy, V., Ocsovszki, I., et al. (2021) · The Journal of Steroid Biochemistry and Molecular Biology · doi:10.1016/j.jsbmb.2021.105997 · Cited by 13 · see citing works
Samartzis, E. P., Imesch, P., Twiehaus, A., Dubey, R. K., & Leeners, B. (2016) · Gynecological Endocrinology · doi:10.3109/09513590.2015.1137094 · Cited by 13 · see citing works
“expressed in endometriotic tissue and disease-free endometrium lacks aromatase expression [4,5].”
BackgroundWołuń-Cholewa, M., Szymanowski, K., Nowak‐Markwitz, E., et al. (2011) · Photodiagnosis and Photodynamic Therapy · doi:10.1016/j.pdpdt.2010.12.003 · Cited by 13 · see citing works
da Costa, K. D. A., Malvezzi, H., Dobo, C., Neme, R. M., Filippi, R. Z., Aloia, T. P. A., Prado, E. R., Meola, J., & Piccinato, C. D. A. (2022) · Frontiers in Molecular Biosciences · doi:10.3389/fmolb.2022.854991 · Cited by 15 · see citing works
“Expression of reducing type- HSD17B1 mRNA was significantly higher in the ectopic tissue (superficial peritoneal endometriosis: SUP, DIE, and OMA), whereas no difference was seen in the expression of HSD17B1-oxidizing types 2 and 4 (Šmuc et al., 2007; Bulun et al., 2010; Delvoux et al., 2014).”
BackgroundSULFATION PATHWAYS: Contribution of intracrine oestrogens to the aetiology of endometriosis
Piccinato, C. D. A., Malvezzi, H., Gibson, D. A., & Saunders, P. T. K. (2018) · Journal of Molecular Endocrinology · doi:10.1530/jme-17-0297 · Cited by 12 · see citing works
Erraji, H., Ghanmi, A. E., Louanjli, N., Benahmed, M., Mansouri, F. E., Zarqaoui, M., & Ghazi, B. (2025) · Frontiers in Genetics · doi:10.3389/fgene.2025.1597287 · Cited by 11 · see citing works
Endometrial proteomic profile of patients with repeated implantation failure
Yang, J., Wang, L., Ma, J., Diao, L., Chen, J., Cheng, Y., Yang, J., & Li, L. (2023) · Frontiers in Endocrinology · doi:10.3389/fendo.2023.1144393 · Cited by 11 · see citing works
Self-citationMohamed, A., Salah, M., Tahoun, M., Hawner, M., Abdelsamie, A. S., & Frotscher, M. (2022) · Journal of Medicinal Chemistry · doi:10.1021/acs.jmedchem.2c00589 · Cited by 11 · see citing works
Yun, B., Jeon, Y., Seo, S., Park, J. H., Yoon, S., Cho, S., Choi, Y.-S., & Lee, B. (2015) · Reproductive Sciences · doi:10.1177/1933719115589411 · Cited by 10 · see citing works
“019) AIB-1 Glandular cell nucleus Proliferative 30 (10-50) 15 (0-22.”
BackgroundHuang, J., Chen, X., & Liu, J. (2023) · International Immunopharmacology · doi:10.1016/j.intimp.2023.111397 · Cited by 7 · see citing works
Pharmacological Management of Endometriosis-related Pain: The Expert Opinion
Олеговна, Д. С., Berlim, Y. D., Bezhenar, V. F., Станиславович, Г. В., & Baranov, I. I. (2021) · Journal of South Asian Federation of Obstetrics and Gynaecology · doi:10.5005/jp-journals-10006-1838 · Cited by 7 · see citing works
The Structure, Function, and Evaluation of the Female Reproductive Tract
Lessey, B. A., & Young, S. L. (2013) · Elsevier eBooks · doi:10.1016/b978-1-4557-2758-2.00010-x · Cited by 8 · see citing works
Obstetric and perinatal outcomes in women with endometriosis
Rafi, J., Pathiraja, P. D. M., Gelson, E., Brown, R. N., & Alleemudder, D. I. (2022) · The Obstetrician & Gynaecologist · doi:10.1111/tog.12831 · Cited by 7 · see citing works
Widhiantara, I. G., Permatasari, A. A. A. P., Rosiana, I. W., Wiradana, P. A., & Satriyasa, B. K. (2021) · Indian Journal of Forensic Medicine & Toxicology · doi:10.37506/ijfmt.v15i4.16914 · Cited by 6 · see citing works
Predictors of illness acceptance in women with endometriosis
Andysz, A., & Merecz‐Kot, D. (2020) · Health Psychology Report · doi:10.5114/hpr.2020.97914 · Cited by 9 · see citing works
Wang, C.-T., Li, C., Wu, W., Huang, C., Li, C., Li, W., Chan, T., Liang, P., Hsing, C., & Liao, K. (2016) · Journal of Cancer · doi:10.7150/jca.16777 · Cited by 6 · see citing works
“The enzyme 17β-hydroxysteroid dehydrogenase type 2 (HSD17B2) plays a vital role in steroid metabolism, including the conversion of the biologically potent factor estradiol into the weakly estrogenic estrone in addition to testosterone and androstenedione [1].”
BackgroundJin, P., Cai, J., Chen, N., Liu, Y., Zhao, H., Wang, Y., Chen, J., Li, M., Xiao, T., Shan, C., et al. (2025) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2025.151964 · Cited by 6 · see citing works
Chen, R., Zhu, H., Zhang, X., Li, L., Xu, J., Tan, Z., Su, J., Feng, K., Chen, K., & Xu, H. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25169063 · Cited by 5 · see citing works
“…in humans and rats reveals that hsd17b2 is the critical steroid downstream element to drive the conversion between active and inactive forms of estrogens and androgens, limiting their active forms in the blood circulation and thus reducing disease risk caused by their abnormal concentration [9].”
BackgroundModern view on the pathogenesis of proliferative diseases of the uterus
Bazhenova, L., Shramko, S., Sabantsev, M. A., & Gulyaeva, L. (2018) · Russian Bulletin of Obstetrician-Gynecologist · doi:10.17116/rosakush20181806131 · Cited by 2 · see citing works
Signaling Pathways in Endometriosis (Eutopic/Ectopic)
Kim, J. J., & Yin, X. (2011) · doi:10.1002/9781444398519.ch16 · Cited by 4 · see citing works
El‐Shalofy, A. S., Wagener, K., Weber, K., Blanco, M., Bauersachs, S., & Bollwein, H. (2021) · Reproductive Biology · doi:10.1016/j.repbio.2021.100577 · Cited by 3 · see citing works
Mousazadeh, S., Ghaheri, A., Shahhoseini, M., Aflatoonian, R., & Afsharian, P. (2019) · International Journal of Reproductive BioMedicine (IJRM) · doi:10.18502/ijrm.v17i3.4517 · Cited by 3 · see citing works
“This defect causes the deficient metabolism of E2 and increases local concentrations of E2 in endometriosis (20).”
BackgroundEtiologies of endometriosis and model systems: is there a risk of a tunnel vision?
Manavalan, M. A., Babtain, M., Weessies, M., Nap, A. W., Verdurmen, W. P. R., Taurin, S., Sater, M. S., & Brock, R. E. (2025) · Frontiers in Medicine · doi:10.3389/fmed.2025.1675051 · Cited by 3 · see citing works
Tolerability and Shared Decision-Making in the Hormonal Management of Endometriosis-Associated Pain
Viana, D. P. D. C., Jacobsen, L., Mota, I. L. P., Comin, A., Correia, E. L. D. S., Fernandes, D. D. M., & Dias, A. C. P. (2025) · Biomedicines · doi:10.3390/biomedicines13092294 · Cited by 5 · see citing works
Li, Q., Dai, Y., Li, X., Wu, Y., Gu, Z., Zhang, C., Yan, H., Lyu, S., Zhang, B., Shi, J., et al. (2024) · Reproductive BioMedicine Online · doi:10.1016/j.rbmo.2024.104393 · Cited by 3 · see citing works
Retinoid Metabolism in Endometriosis
Çakıroğlu, Y., Confino, R., & Pavone, M. E. (2017) · Journal of Endometriosis and Pelvic Pain Disorders · doi:10.5301/jeppd.5000309 · Cited by 2 · see citing works
“J Endometr Pelvic Pain Disord 2017; 9(4): 232-238 JEPPD”
BackgroundSelf-citationNemeti, G. I., Craciun, A. E., Măgureanu, D. C., Militaru, F. C., Bocșan, I. C., Crăciun, C.-I., Rusu, A., Melincovici, C. S., Buzoianu, A. D., Mureșan, D., et al. (2026) · International Journal of Molecular Sciences · doi:10.3390/ijms27114883 · Cited by 3 · see citing works
Coutinho, L. M., Bernacchioni, C., Casalechi, M., Vannuccini, S., Francisco, A. M. C., Petraglia, F., & dos Reis, F. M. (2024) · Journal of Endometriosis and Uterine Disorders · doi:10.1016/j.jeud.2024.100093 · Cited by 1 · see citing works
Pullen, N. (2012) · InTech eBooks · doi:10.5772/29021 · Cited by 1 · see citing works
“compartment (Bulun et al., 2010; Zeitoun et al., 1998).”
BackgroundKhalmirzaeva, M., Omarova, G., Kurmanova, А., Kurmanova, G., Anartayeva, G., Zhankina, Z., Tulesheva, A., Veliyeva, A., Jarikova, B., & Dzheksembekova, A. Y. (2026) · Biomedicines · doi:10.3390/biomedicines14071560
Goyal, R. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.05.27.728028
Effect of high-intensity focused ultrasound ablation on lesion stiffness and symptoms of adenomyosis
Shen, X., Chen, W. W., Shi, Q., Zi, D., Ren, X., & Tian, X. (2026) · International Journal of Hyperthermia · doi:10.1080/02656736.2026.2642927 · Cited by 1 · see citing works
Potential Changes in the Eutopic Endometrium in Endometriosis: A Narrative Review
Makrygiannakis, F., Vrekoussis, T., Berdiaki, A., & Makrigiannakis, A. (2025) · Cureus · doi:10.7759/cureus.92932
“An imbalance between 17 β -hydroxysteroid dehydrogenase type 1 and 2 has been reported in endometriotic cells, with 17 β -hydroxysteroid dehydrogenase type 2 being significantly down-regulated [28,29].”
PREGNANCY COMPLICATIONS IN PATIENTS WITH ENDOMETRIOSIS
Sulukhia, R., Melia, L., DAVIDOVA, N., & Pkhaladze, L. (2023) · EXPERIMENTAL & CLINICAL MEDICINE GEORGIA · doi:10.52340/jecm.2023.05.26
Rolla, E. D. (2021) · Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature · doi:10.3410/f.740035280.793585488
Initiation and progression of Mullerian duct derived malignancies
van der Horst, P. (2013)
Bragança, C. M. C. (2013) · Portuguese National Funding Agency for Science, Research and Technology (RCAAP Project by FCT) · doi:10.34626/2fxe-we94
Salmeri, V. S. F. M. (2013) · Journal of Pain & Relief · doi:10.4172/2167-0846.1000123
“This fail is probably related to overall reduction in the levels of progesterone receptors (PRs) and, in particular, to the lack of the PR isoform B (PR-B) typical of endometriotic implants [35].”
BackgroundEndométriose : pourquoi se développe-telle ?
Béliard, A., Foidart, J.-M., & Nisolle, M. (2012) · Open Repository and Bibliography (University of Liège)
Sokalska, A., & Dulęba, A. J. (2011) · doi:10.1002/9781444398519.ch36
- Authors
- Bulun, S., Cheng, Y.-H., Pavone, M., Yin, P., Imir, G., Utsunomiya, H., Thung, S., Xue, Q., Marsh, E., Tokunaga, H., Ishikawa, H., Kurita, T., & Su, E.
- Affiliations
- Northwestern University (US)
- Tohoku University (JP)
- Yale University (US)
- Peking University (CN)
- Chiba University (JP)
- ORCID
- Venue
- Seminars in Reproductive Medicine
- Publisher
- Georg Thieme Verlag KG
- Published
- 2010-01
- Volume
- 28
- Issue
- 01
- Pages
- 044-050
- ISSN
- 1526-4564 (ISSN-L)
- 1526-8004
- PMC
- PMC4511594
- OpenAlex
- W2017522870
- Cited by
- 86
- References
- 34
- Citations by year
- 2026: 4 · 2025: 5 · 2024: 5 · 2023: 5 · 2022: 6 · 2021: 11 · 2020: 3 · 2019: 4 · 2018: 4 · 2017: 6 · 2016: 3 · 2015: 2 · 2014: 3 · 2013: 6 · 2012: 8
- FWCI
- 9.48
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Seminars in Reproductive Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (HD038691, R01HD038691, R37HD038691)
- Topics
- Health Sciences › Medicine › Reproductive Medicine › Endometriosis Research and Treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Ectopic Pregnancy Diagnosis and Management
- Keywords
- endometriosis, 17β-hydroxysteroid dehydrogenase type 2, HSD17B2, progesterone resistance, progesterone receptor, estradiol metabolism, estrone, endometriotic stromal cells, paracrine signaling, endometrium
- MeSH terms
- Animals, Cell Differentiation, Endometriosis, Female, Gene Expression Regulation, Humans, Progesterone, Receptors, Progesterone, 17-Hydroxysteroid Dehydrogenases, Stromal Cells, Paracrine Communication, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Claims read under definition version 3 (extract-v3) on 2026-09-28.
Classified by jev-1.13-20260917 (gold-guideline-v0.2) on 2026-09-28.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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