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Endometriosis Triggers Excessive Activation of Primordial Follicles via PI3K-PTEN-Akt-Foxo3 Pathway
Abstract
Context The ovarian reserve is reduced in patients with endometriosis. We hypothesize that the phosphatidylinositol 3-kinase (PI3K)-phosphatase and tensin homolog deleted on chromosome 10 (PTEN) Akt-Forkhead box O (Foxo3) pathway is involved in reducing the ovarian reserve. Objective To elucidate the signaling mechanism by which endometriosis decreases ovarian reserve. Design Studies were conducted by using a mouse model for endometriosis and human ovaries. The endometriosis mouse model was established and ammonium trichloro (dioxoethylene-o,o') tellurate (AS101), an inhibitor of PI3K-PTEN-Akt pathway, was administered to experimental mice. Human ovaries were collected during surgery from patients with endometrioma or from patients with no ovarian pathology (control ovaries). The number of follicles and expression of Foxo3, PTEN, phosphorylated mammalian target of rapamycin and phosphorylated Akt by oocytes in primordial follicles in mouse and human ovaries were detected by immunohistochemical staining and evaluated. Results In the endometriosis mouse model, the proportion of primordial follicles was diminished, and the proportion of primary, secondary, antral, and growing follicles was increased in comparison with controls. In both mouse and human ovaries, the PI3K-PTEN-Akt-Foxo3 pathway was activated in samples from endometriosis. Administration of AS101 restored the proportion of primordial follicles in endometriotic mice ovaries to control levels. Conclusions The current…
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In ovaries affected by endometriosis, a higher proportion of primordial follicles are recruited into the growing pool and a greater number of maturing follicles degenerate, resulting in quicker depletion of ovarian reserve.
“In ovaries affected by endometriosis, a higher proportion of primordial follicles are recruited into the growing pool and a greater number of maturing follicles degenerate, resulting in quicker depletion of ovarian reserve (Kitajima et al., 2014; Takeuchi et al., 2019).”
From Endometriosis and polycystic ovary syndrome are diametric disorders (2021) · cites this paper as Takeuchi et al., 2019
Endometriosis is associated with lower ovarian reserve, increased primordial follicle recruitment, fewer antral follicles, and a steeper rate of decline in AMH.
“Endometriosis, by contrast, is associated with lower ovarian reserve (Seyhan et al., 2015; Shah, 2013), increased primordial follicle recruitment (Takeuchi et al., 2019), fewer antral follicles (Muzii et al., 2018), and a steeper rate of decline in AMH (Kasapoglu et al., 2018).”
From Endometriosis and polycystic ovary syndrome are diametric disorders (2021) · cites this paper as Takeuchi et al., 2019
Lower testosterone in women with endometriosis contributes to a faster pace of follicular recruitment and death.
“Lower testosterone in women with endometriosis shows evidence of contributing to a faster pace of follicular recruitment and death, across several studies.”
From Endometriosis and polycystic ovary syndrome are diametric disorders (2021) · cites this paper as Takeuchi et al., 2019
Citations
Cites
AMPK regulates energy expenditure by modulating NAD+ metabolism and SIRT1 activity
Cantó, C., Gerhart-Hines, Z., Feige, J. N., Lagouge, M., Noriega, L., Milne, J. C., Elliott, P. J., Puigserver, P., & Auwerx, J. (2009) · Nature · doi:10.1038/nature07813 · Cited by 3,300
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Research works printed but not linked: 21
- Zondervan, 2018, Endometriosis, Nat Rev Dis Primers, 4, 9, 10.1038/s41572-018-0008-5 · DOI · Paper page
- Muzii, 2018, Antimüllerian hormone is reduced in the presence of ovarian endometriomas: a systematic review and meta-analysis, Fertil Steril, 110, 932, 10.1016/j.fertnstert.2018.06.025 · DOI · Paper page
- Kasapoglu, 2018, Endometrioma-related reduction in ovarian reserve (ERROR): a prospective longitudinal study, Fertil Steril, 110, 122, 10.1016/j.fertnstert.2018.03.015 · DOI · Paper page
- Ashrafi, 2019, The impact of the localisation of endometriosis lesions on ovarian reserve and assisted reproduction techniques outcomes, J Obstet Gynaecol, 39, 91-797, 10.1080/01443615.2018.1465898 · DOI
- Dolmans, 2007, Short-term transplantation of isolated human ovarian follicles and cortical tissue into nude mice, Reproduction, 134, 253, 10.1530/REP-07-0131 · DOI
- Kitajima, 2014, Enhanced follicular recruitment and atresia in cortex derived from ovaries with endometriomas, Fertil Steril, 101, 1031, 10.1016/j.fertnstert.2013.12.049 · DOI · Paper page
- Castrillon, 2003, Suppression of ovarian follicle activation in mice by the transcription factor Foxo3a, Science, 301, 215, 10.1126/science.1086336 · DOI
- Liu, 2007, Infertility caused by retardation of follicular development in mice with oocyte-specific expression of Foxo3a, Development, 134, 199, 10.1242/dev.02667 · DOI
- Pelosi, 2013, Constitutively active Foxo3 in oocytes preserves ovarian reserve in mice, Nat Commun, 4, 1843, 10.1038/ncomms2861 · DOI
- Adhikari, 2010, mTOR signaling in the control of activation of primordial follicles, Cell Cycle, 9, 1673, 10.4161/cc.9.9.11626 · DOI
- Jagarlamudi, 2012, Oogenesis: transcriptional regulators and mouse models, Mol Cell Endocrinol, 356, 31, 10.1016/j.mce.2011.07.049 · DOI
- Takamura, 2016, Neutrophil depletion reduces endometriotic lesion formation in mice, Am J Reprod Immunol, 76, 193, 10.1111/aji.12540 · DOI · Paper page
- Kalich-Philosoph, 2013, Cyclophosphamide triggers follicle activation and “burnout”; AS101 prevents follicle loss and preserves fertility, Sci Transl Med, 5, 185ra62, 10.1126/scitranslmed.3005402 · DOI
- Myers, 2004, Methods for quantifying follicular numbers within the mouse ovary, Reproduction, 127, 569, 10.1530/rep.1.00095 · DOI
- Chang, 2015, Cisplatin Induces Overactivation of the Dormant Primordial Follicle through PTEN/AKT/FOXO3a Pathway which Leads to Loss of Ovarian Reserve in Mice, PLoS One, 10, e0144245, 10.1371/journal.pone.0144245 · DOI
- Sonigo, 2019, AMH prevents primordial ovarian follicle loss and fertility alteration in cyclophosphamide-treated mice, FASEB J, 33, 1278, 10.1096/fj.201801089R · DOI
- McKinnon, 2016, Kinase signalling pathways in endometriosis: potential targets for non-hormonal therapeutics, Hum Reprod Update, 22, 382, 10.1093/humupd/dmv060 · DOI
- Leconte, 2011, The mTOR/AKT inhibitor temsirolimus prevents deep infiltrating endometriosis in mice, Am J Pathol, 179, 880, 10.1016/j.ajpath.2011.04.020 · DOI
- Matsuzaki, 2018, In vitro and in vivo effects of MK2206 and chloroquine combination therapy on endometriosis: autophagy may be required for regrowth of endometriosis, Br J Pharmacol, 175, 1637, 10.1111/bph.14170 · DOI
- Barra, 2018, Inhibition of PI3K/AKT/mTOR pathway for the treatment of endometriosis, Br J Pharmacol, 175, 3626, 10.1111/bph.14391 · DOI
- Esposito, Safety, tolerability, and management of toxic effects of phosphatidylinositol 3-kinase inhibitor treatment in patients with cancer: a review [published online ahead of print 28 March 2019], JAMA Oncol
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Endometriosis and polycystic ovary syndrome are diametric disorders
Dinsdale, N. L., & Crespi, B. J. (2021) · Evolutionary Applications · doi:10.1111/eva.13244 · Cited by 90
“In ovaries affected by endometriosis, a higher proportion of primordial follicles are recruited into the growing pool and a greater number of maturing follicles degenerate, resulting in quicker depletion of ovarian reserve (Kitajima et al., 2014; Takeuchi et al., 2019).”
BackgroundThe evolutionary biology of endometriosis
Dinsdale, N., Nepomnaschy, P., & Crespi, B. (2021) · Evolution, Medicine, and Public Health · doi:10.1093/emph/eoab008 · Cited by 53
Metadata
- Authors
- Takeuchi, A., Koga, K., Satake, E., Makabe, T., Taguchi, A., Miyashita, M., Takamura, M., Harada, M., Hirata, T., Hirota, Y., Yoshino, O., Wada-Hiraike, O., Fujii, T., & Osuga, Y.
- Affiliations
- The University of Tokyo (JP)
- Obstetrics and Gynecology, University of Tokyo, Hongo Bunkyo Tokyo, Japan
- Kitasato University (JP)
- Corresponding author
- Koga, Kaori
- ORCID
- Venue
- The Journal of Clinical Endocrinology & Metabolism
- Publisher
- The Endocrine Society
- Published
- 2019-06-20
- Volume
- 104
- Issue
- 11
- Pages
- 5547-5554
- ISSN
- 0021-972X (ISSN-L)
- 1945-7197
- OpenAlex
- W2951322526
- Cited by
- 68
- References
- 1
- Citations by year
- 2026: 7 · 2025: 14 · 2024: 14 · 2023: 9 · 2022: 9 · 2021: 9 · 2020: 5 · 2019: 1
- FWCI
- 5.97
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The Journal of Clinical Endocrinology & Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Japan Agency for Medical Research and Development (197100000040)
- Japan Society for the Promotion of Science (187100000421)
- Yamaguchi Endocrine Research Foundation (NA)
- Shiseido Group (NA)
- Society for Women's Health Science Research (NA)
- Kanzawa Medical Research Foundation (NA)
- Topics
- Health Sciences › Medicine › Reproductive Medicine › Endometriosis Research and Treatment
- Health Sciences › Medicine › Reproductive Medicine › Reproductive Biology and Fertility
- Health Sciences › Medicine › Reproductive Medicine › Ovarian function and disorders
- Keywords
- endometriosis, ovarian reserve, primordial follicles, FOXO3, AS101, PI3K inhibitors, endometrioma, folliculogenesis, mTOR, Akt phosphorylation
- MeSH terms
- Forkhead Box Protein O3, Animals, Disease Models, Animal, Endometriosis, Female, Ovarian Follicle, Humans, Ovary, Phosphorylation, Signal Transduction, Phosphatidylinositol 3-Kinases, Proto-Oncogene Proteins c-akt, PTEN Phosphohydrolase, Mice
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