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Современные молекулярно-биологические аспекты эндометриоз-ассоциированного бесплодия
Современные молекулярно-биологические аспекты эндометриоз-ассоциированного бесплодия
Сафронова А.С., Высоких М.Ю., Чупрынин В.Д., Буралкина Н.А. Современные молекулярно-биологические аспекты эндометриоз-ассоциированного бесплодия. Гинекология. 2019; 21 (5): 12–15.
DOI: 10.26442/20795696.2019.5.190731
DOI: 10.26442/20795696.2019.5.190731
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Аннотация
В настоящее время не существует консенсуса в вопросе этиопатогенетической природы эндометриоза. Причины агрессивного прогрессирующего инфильтративного роста эндометриоидной ткани также неясны. Важной проблемой остается высокая частота рецидивов эндометриоза, несмотря на наличие современных медикаментозных и хирургических методов лечения. Изучение центральных сигнальных путей и поиск новых ключевых молекул имеют первостепенное значение для лучшего понимания патогенеза заболевания, а также являются важным шагом в разработке новых стратегий диагностики, профилактики и лечения эндометриоза.
Ключевые слова: глубокий инфильтративный эндометриоз, патогенез эндометриоза, биомаркеры, сигнальные пути.
Key words: deep infiltrative endometriosis, pathogenesis of endometriosis, biomarkers, signaling pathways.
Ключевые слова: глубокий инфильтративный эндометриоз, патогенез эндометриоза, биомаркеры, сигнальные пути.
________________________________________________
Key words: deep infiltrative endometriosis, pathogenesis of endometriosis, biomarkers, signaling pathways.
Полный текст
Список литературы
1. Минздрав России. Заболеваемость населения России в 2010–2017 гг. Статистические материалы. Часть IV, Москва, 2011–2018 гг. Справочно-информационные материалы службы охраны здоровья матери и ребенка, Москва, с 2005 г. М., 2018.
[Ministry of Health. Morbidity of the population of Russia in 2010–2017 Statistical materials. Part IV, Moscow, 2011–2018 reference and information materials of the maternal and child health service, Moscow, since 2005. Moscow, 2018 (in Russian).]
2. Bendifallah S, Roman H, Mathieu d’Argent E et al. Colorectal endometriosis-associated infertility: should surgery precede ART? Fertil Stiril 2017; 108 (3): 525–31.
3. Darai E, Cohen J, Ballester M. Colorectal endometriosis and fertility. Eur J Obstet Gynecol Reprod Biol 2017; 209: 86–94.
4. Wang L, Zhao J, Li Y et al. Genome-wide analysis of DNA methylation in endometriosis using Illumina Human Methylation 450 K BeadChips. Mol Reprod Dev 2019; 1–11. https://doi.org/10.1002/mrd.23127
5. Баскаков В.П, Цвелев Ю.В., Кира Е.Ф. Эндометриоидная болезнь. СПб.: Издательство Н-Л, 2002.
[Baskakov V.P, Tsvelev Iu.V., Kira E.F. Endometrioid disease. Saint Petersburg: Izdatel'stvo N-L, 2002 (in Russian).]
6. Закиян С.М., Власова В.В., Дементьева Е.В. Эпигенетика. М.: СО РАН, 2012.
[Zakiian S.M., Vlasova V.V., Dement'eva E.V. Epigenetics. Moscow: SO RAN, 2012 (in Russian).]
7. Адамян Л.В., Азнаурова Я.Б. Молекулярные аспекты патогенеза эндометриоза. Проблемы репродукции. 2015; 2: 66–77.
[Adamian L.V., Aznaurova Ia.B. Molekuliarnye aspekty patogeneza endometrioza. Problemy reproduktsii. 2015; 21 (2): 66–77 (in Russian).]
8. Liu Z, Yi L, Du M et al. Overexpression of TGF-b enhances the migration and invasive ability of ectopic endometrial cells via ERK/MAPK signaling pathway. Exp Therapeutic Med 2019; 17: 4457–64.
9. Hoque R, Malik AF, Gorelick F, Mehal WZ. Sterile inflammatory response in acute pancreatitis. Pancreas 2012; 41: 353–7.
10. Kajihara H, Yamada Y, Kanayama S et al. New insights into the pathophysiology of endometriosis: from chronic inflammation to danger signal. Gynecol Endocrinol 2011; 27: 73–9.
11. Ельчанинов А.В., Фатхудинов Т.Х., Кананыхина Е.Ю. и др. Активность генов NOTCH-сигнального пути и NOTCH-зависимых генов в печени крыс после субтотальной резекции. Гены&Клетки. 2016; 11 (3): 40–6.
[El'chaninov A.V., Fatkhudinov T.Kh., Kananykhina E.Yu. et al. Aktivnost' genov NOTCH-signal'nogo puti i NOTCH-zavisimykh genov v pecheni krys posle subtotal'noi rezektsii. Geny&Kletki. 2016; 11 (3): 40–6 (in Russian).]
12. Kobayashi H, Higashiura Y, Shigetomi H, Kajihara H. Pathogenesis of endometriosis: The role of initial infection and subsequent sterile inflammation (Review). Mol Med Rep 2014; 9: 9–15. https://doi.org/10.3892/mmr.2013.1755
13. Invitti AL, Schor E, Parreira RM et al. Inflammatory cytokine profile of co cultivated primary cells from the endometrium of women with and without endometriosis. Mol Med Rep 2018; 18: 1287–96.
14. Durmus AB, Cengiz SD, Yilmaz H et al. The levels of matrix metalloproteinase-9 and neutrophil gelatinase-associated lipocalin in different stages of endometriosis. J Obstetrics Gynaecol 2019; 39 (7): 991–5. DOI: 10.1080/01443615.2019.1584889
15. Ferreira EM, Giorgi VSI, Rodrigues JK et al. Systemic oxidative stress in the early follicular phase as a possible mechanism underlying the pathogenesis of mild endometriosis-related infertility and a helpful tool to predict ICSI outcomes: a pilot study. Reprod BioMed Online 2019; 39 (5): 785–94. DOI: https://doi.org/10.1016/j.rbmo.2019.06.011
16. Nisenblat V, Bossuyt P, Shaikh R et al. Blood biomarkers for the non-invasive diagnosis of endometriosis (Review). Cochrane Database Syst Rev 2016; 5: CD012179.
17. González-Foruria I, Santulli P, Chouzenoux S et al. Dysregulation of the ADAM17/Notch signalling pathways in endometriosis: from oxidative stress to fibrosis. Mol Human Reprod 2017; 23 (7): 488–99.
18. Kavian N, Servettaz A, Mongaret C et al. Targeting ADAM-17/notch signaling abrogates the development of systemic sclerosis in a murine model. Arthritis Rheum 2010: 62 (11): 3477–87.
19. Sua R-W, Struga MR, Jeonga J-W et al. Aberrant activation of canonical Notch1 signaling in the mouse uterus decreases progesterone receptor by hypermethylation and leads to infertility. Proc Natl Acad Sci 2016; 113 (8): 2300–5.
20. Su RW, Strug MR, Joshi NR et al. Decreased Notch pathway signaling in the endometrium of women with endometriosis impairs decidualization. J Clin Endocrinol Metab 2015; 100 (3): E433–E442.
21. Bulun SE, Cheng YH, Yin P et al. Progesterone resistance in endometriosis: link to failure to metabolize estradiol. Mol Cell Endocrinol 2006; 248: 94–103.
22. Chae U, Min JY, Kim SH et al. Decreased Progesterone Receptor B/A Ratio in Endometrial Cells by Tumor Necrosis Factor-Alpha and Peritoneal Fluid from Patients with Endometriosis. Yonsei Med J 2016; 57 (6): 1468–74.
23. Bulun SE, Monsavais D, Pavone ME et al. Role of estrogen receptor-beta in endometriosis. Semin Reprod Med 2012; 30: 39–45.
24. Lessey BA, Lebovic DI, Taylor RN. Eutopic endometrium in women with endometriosis: ground zero for the study of implantation defects. Semin Reprod Med 2013; 31: 109–24.
25. Liao T, Lee Y-C, Tzeng C-R et al. Mitochondrial translocation of estrogen receptor-b affords resistance to oxidative insult-induced apoptosis and contributes to the pathogenesis of endometriosis. Free Radic Biol Med 2019; 134: 359–73.
26. Nisenblat V, Prentice L, Bossuyt P et al. Combination of the non-invasive tests for the diagnosis of endometriosis (Review). Cochrane Database Syst Rev 2016; 7: CD012281.
2. Bendifallah S, Roman H, Mathieu d’Argent E et al. Colorectal endometriosis-associated infertility: should surgery precede ART? Fertil Stiril 2017; 108 (3): 525–31.
3. Darai E, Cohen J, Ballester M. Colorectal endometriosis and fertility. Eur J Obstet Gynecol Reprod Biol 2017; 209: 86–94.
4. Wang L, Zhao J, Li Y et al. Genome-wide analysis of DNA methylation in endometriosis using Illumina Human Methylation 450 K BeadChips. Mol Reprod Dev 2019; 1–11. https://doi.org/10.1002/mrd.23127
5. Baskakov V.P, Tsvelev Iu.V., Kira E.F. Endometrioid disease. Saint Petersburg: Izdatel'stvo N-L, 2002 (in Russian).
6. Zakiian S.M., Vlasova V.V., Dement'eva E.V. Epigenetics. Moscow: SO RAN, 2012 (in Russian).
7. Adamian L.V., Aznaurova Ia.B. Molekuliarnye aspekty patogeneza endometrioza. Problemy reproduktsii. 2015; 21 (2): 66–77 (in Russian).
8. Liu Z, Yi L, Du M et al. Overexpression of TGF-b enhances the migration and invasive ability of ectopic endometrial cells via ERK/MAPK signaling pathway. Exp Therapeutic Med 2019; 17: 4457–64.
9. Hoque R, Malik AF, Gorelick F, Mehal WZ. Sterile inflammatory response in acute pancreatitis. Pancreas 2012; 41: 353–7.
10. Kajihara H, Yamada Y, Kanayama S et al. New insights into the pathophysiology of endometriosis: from chronic inflammation to danger signal. Gynecol Endocrinol 2011; 27: 73–9.
11. El'chaninov A.V., Fatkhudinov T.Kh., Kananykhina E.Yu. et al. Aktivnost' genov NOTCH-signal'nogo puti i NOTCH-zavisimykh genov v pecheni krys posle subtotal'noi rezektsii. Geny&Kletki. 2016; 11 (3): 40–6 (in Russian).
12. Kobayashi H, Higashiura Y, Shigetomi H, Kajihara H. Pathogenesis of endometriosis: The role of initial infection and subsequent sterile inflammation (Review). Mol Med Rep 2014; 9: 9–15. https://doi.org/10.3892/mmr.2013.1755
13. Invitti AL, Schor E, Parreira RM et al. Inflammatory cytokine profile of co cultivated primary cells from the endometrium of women with and without endometriosis. Mol Med Rep 2018; 18: 1287–96.
14. Durmus AB, Cengiz SD, Yilmaz H et al. The levels of matrix metalloproteinase-9 and neutrophil gelatinase-associated lipocalin in different stages of endometriosis. J Obstetrics Gynaecol 2019; 39 (7): 991–5. DOI: 10.1080/01443615.2019.1584889
15. Ferreira EM, Giorgi VSI, Rodrigues JK et al. Systemic oxidative stress in the early follicular phase as a possible mechanism underlying the pathogenesis of mild endometriosis-related infertility and a helpful tool to predict ICSI outcomes: a pilot study. Reprod BioMed Online 2019; 39 (5): 785–94. DOI: https://doi.org/10.1016/j.rbmo.2019.06.011
16. Nisenblat V, Bossuyt P, Shaikh R et al. Blood biomarkers for the non-invasive diagnosis of endometriosis (Review). Cochrane Database Syst Rev 2016; 5: CD012179.
17. González-Foruria I, Santulli P, Chouzenoux S et al. Dysregulation of the ADAM17/Notch signalling pathways in endometriosis: from oxidative stress to fibrosis. Mol Human Reprod 2017; 23 (7): 488–99.
18. Kavian N, Servettaz A, Mongaret C et al. Targeting ADAM-17/notch signaling abrogates the development of systemic sclerosis in a murine model. Arthritis Rheum 2010: 62 (11): 3477–87.
19. Sua R-W, Struga MR, Jeonga J-W et al. Aberrant activation of canonical Notch1 signaling in the mouse uterus decreases progesterone receptor by hypermethylation and leads to infertility. Proc Natl Acad Sci 2016; 113 (8): 2300–5.
20. Su RW, Strug MR, Joshi NR et al. Decreased Notch pathway signaling in the endometrium of women with endometriosis impairs decidualization. J Clin Endocrinol Metab 2015; 100 (3): E433–E442.
21. Bulun SE, Cheng YH, Yin P et al. Progesterone resistance in endometriosis: link to failure to metabolize estradiol. Mol Cell Endocrinol 2006; 248: 94–103.
22. Chae U, Min JY, Kim SH et al. Decreased Progesterone Receptor B/A Ratio in Endometrial Cells by Tumor Necrosis Factor-Alpha and Peritoneal Fluid from Patients with Endometriosis. Yonsei Med J 2016; 57 (6): 1468–74.
23. Bulun SE, Monsavais D, Pavone ME et al. Role of estrogen receptor-beta in endometriosis. Semin Reprod Med 2012; 30: 39–45.
24. Lessey BA, Lebovic DI, Taylor RN. Eutopic endometrium in women with endometriosis: ground zero for the study of implantation defects. Semin Reprod Med 2013; 31: 109–24.
25. Liao T, Lee Y-C, Tzeng C-R et al. Mitochondrial translocation of estrogen receptor-b affords resistance to oxidative insult-induced apoptosis and contributes to the pathogenesis of endometriosis. Free Radic Biol Med 2019; 134: 359–73.
26. Nisenblat V, Prentice L, Bossuyt P et al. Combination of the non-invasive tests for the diagnosis of endometriosis (Review). Cochrane Database Syst Rev 2016; 7: CD012281.
[Ministry of Health. Morbidity of the population of Russia in 2010–2017 Statistical materials. Part IV, Moscow, 2011–2018 reference and information materials of the maternal and child health service, Moscow, since 2005. Moscow, 2018 (in Russian).]
2. Bendifallah S, Roman H, Mathieu d’Argent E et al. Colorectal endometriosis-associated infertility: should surgery precede ART? Fertil Stiril 2017; 108 (3): 525–31.
3. Darai E, Cohen J, Ballester M. Colorectal endometriosis and fertility. Eur J Obstet Gynecol Reprod Biol 2017; 209: 86–94.
4. Wang L, Zhao J, Li Y et al. Genome-wide analysis of DNA methylation in endometriosis using Illumina Human Methylation 450 K BeadChips. Mol Reprod Dev 2019; 1–11. https://doi.org/10.1002/mrd.23127
5. Баскаков В.П, Цвелев Ю.В., Кира Е.Ф. Эндометриоидная болезнь. СПб.: Издательство Н-Л, 2002.
[Baskakov V.P, Tsvelev Iu.V., Kira E.F. Endometrioid disease. Saint Petersburg: Izdatel'stvo N-L, 2002 (in Russian).]
6. Закиян С.М., Власова В.В., Дементьева Е.В. Эпигенетика. М.: СО РАН, 2012.
[Zakiian S.M., Vlasova V.V., Dement'eva E.V. Epigenetics. Moscow: SO RAN, 2012 (in Russian).]
7. Адамян Л.В., Азнаурова Я.Б. Молекулярные аспекты патогенеза эндометриоза. Проблемы репродукции. 2015; 2: 66–77.
[Adamian L.V., Aznaurova Ia.B. Molekuliarnye aspekty patogeneza endometrioza. Problemy reproduktsii. 2015; 21 (2): 66–77 (in Russian).]
8. Liu Z, Yi L, Du M et al. Overexpression of TGF-b enhances the migration and invasive ability of ectopic endometrial cells via ERK/MAPK signaling pathway. Exp Therapeutic Med 2019; 17: 4457–64.
9. Hoque R, Malik AF, Gorelick F, Mehal WZ. Sterile inflammatory response in acute pancreatitis. Pancreas 2012; 41: 353–7.
10. Kajihara H, Yamada Y, Kanayama S et al. New insights into the pathophysiology of endometriosis: from chronic inflammation to danger signal. Gynecol Endocrinol 2011; 27: 73–9.
11. Ельчанинов А.В., Фатхудинов Т.Х., Кананыхина Е.Ю. и др. Активность генов NOTCH-сигнального пути и NOTCH-зависимых генов в печени крыс после субтотальной резекции. Гены&Клетки. 2016; 11 (3): 40–6.
[El'chaninov A.V., Fatkhudinov T.Kh., Kananykhina E.Yu. et al. Aktivnost' genov NOTCH-signal'nogo puti i NOTCH-zavisimykh genov v pecheni krys posle subtotal'noi rezektsii. Geny&Kletki. 2016; 11 (3): 40–6 (in Russian).]
12. Kobayashi H, Higashiura Y, Shigetomi H, Kajihara H. Pathogenesis of endometriosis: The role of initial infection and subsequent sterile inflammation (Review). Mol Med Rep 2014; 9: 9–15. https://doi.org/10.3892/mmr.2013.1755
13. Invitti AL, Schor E, Parreira RM et al. Inflammatory cytokine profile of co cultivated primary cells from the endometrium of women with and without endometriosis. Mol Med Rep 2018; 18: 1287–96.
14. Durmus AB, Cengiz SD, Yilmaz H et al. The levels of matrix metalloproteinase-9 and neutrophil gelatinase-associated lipocalin in different stages of endometriosis. J Obstetrics Gynaecol 2019; 39 (7): 991–5. DOI: 10.1080/01443615.2019.1584889
15. Ferreira EM, Giorgi VSI, Rodrigues JK et al. Systemic oxidative stress in the early follicular phase as a possible mechanism underlying the pathogenesis of mild endometriosis-related infertility and a helpful tool to predict ICSI outcomes: a pilot study. Reprod BioMed Online 2019; 39 (5): 785–94. DOI: https://doi.org/10.1016/j.rbmo.2019.06.011
16. Nisenblat V, Bossuyt P, Shaikh R et al. Blood biomarkers for the non-invasive diagnosis of endometriosis (Review). Cochrane Database Syst Rev 2016; 5: CD012179.
17. González-Foruria I, Santulli P, Chouzenoux S et al. Dysregulation of the ADAM17/Notch signalling pathways in endometriosis: from oxidative stress to fibrosis. Mol Human Reprod 2017; 23 (7): 488–99.
18. Kavian N, Servettaz A, Mongaret C et al. Targeting ADAM-17/notch signaling abrogates the development of systemic sclerosis in a murine model. Arthritis Rheum 2010: 62 (11): 3477–87.
19. Sua R-W, Struga MR, Jeonga J-W et al. Aberrant activation of canonical Notch1 signaling in the mouse uterus decreases progesterone receptor by hypermethylation and leads to infertility. Proc Natl Acad Sci 2016; 113 (8): 2300–5.
20. Su RW, Strug MR, Joshi NR et al. Decreased Notch pathway signaling in the endometrium of women with endometriosis impairs decidualization. J Clin Endocrinol Metab 2015; 100 (3): E433–E442.
21. Bulun SE, Cheng YH, Yin P et al. Progesterone resistance in endometriosis: link to failure to metabolize estradiol. Mol Cell Endocrinol 2006; 248: 94–103.
22. Chae U, Min JY, Kim SH et al. Decreased Progesterone Receptor B/A Ratio in Endometrial Cells by Tumor Necrosis Factor-Alpha and Peritoneal Fluid from Patients with Endometriosis. Yonsei Med J 2016; 57 (6): 1468–74.
23. Bulun SE, Monsavais D, Pavone ME et al. Role of estrogen receptor-beta in endometriosis. Semin Reprod Med 2012; 30: 39–45.
24. Lessey BA, Lebovic DI, Taylor RN. Eutopic endometrium in women with endometriosis: ground zero for the study of implantation defects. Semin Reprod Med 2013; 31: 109–24.
25. Liao T, Lee Y-C, Tzeng C-R et al. Mitochondrial translocation of estrogen receptor-b affords resistance to oxidative insult-induced apoptosis and contributes to the pathogenesis of endometriosis. Free Radic Biol Med 2019; 134: 359–73.
26. Nisenblat V, Prentice L, Bossuyt P et al. Combination of the non-invasive tests for the diagnosis of endometriosis (Review). Cochrane Database Syst Rev 2016; 7: CD012281.
________________________________________________
2. Bendifallah S, Roman H, Mathieu d’Argent E et al. Colorectal endometriosis-associated infertility: should surgery precede ART? Fertil Stiril 2017; 108 (3): 525–31.
3. Darai E, Cohen J, Ballester M. Colorectal endometriosis and fertility. Eur J Obstet Gynecol Reprod Biol 2017; 209: 86–94.
4. Wang L, Zhao J, Li Y et al. Genome-wide analysis of DNA methylation in endometriosis using Illumina Human Methylation 450 K BeadChips. Mol Reprod Dev 2019; 1–11. https://doi.org/10.1002/mrd.23127
5. Baskakov V.P, Tsvelev Iu.V., Kira E.F. Endometrioid disease. Saint Petersburg: Izdatel'stvo N-L, 2002 (in Russian).
6. Zakiian S.M., Vlasova V.V., Dement'eva E.V. Epigenetics. Moscow: SO RAN, 2012 (in Russian).
7. Adamian L.V., Aznaurova Ia.B. Molekuliarnye aspekty patogeneza endometrioza. Problemy reproduktsii. 2015; 21 (2): 66–77 (in Russian).
8. Liu Z, Yi L, Du M et al. Overexpression of TGF-b enhances the migration and invasive ability of ectopic endometrial cells via ERK/MAPK signaling pathway. Exp Therapeutic Med 2019; 17: 4457–64.
9. Hoque R, Malik AF, Gorelick F, Mehal WZ. Sterile inflammatory response in acute pancreatitis. Pancreas 2012; 41: 353–7.
10. Kajihara H, Yamada Y, Kanayama S et al. New insights into the pathophysiology of endometriosis: from chronic inflammation to danger signal. Gynecol Endocrinol 2011; 27: 73–9.
11. El'chaninov A.V., Fatkhudinov T.Kh., Kananykhina E.Yu. et al. Aktivnost' genov NOTCH-signal'nogo puti i NOTCH-zavisimykh genov v pecheni krys posle subtotal'noi rezektsii. Geny&Kletki. 2016; 11 (3): 40–6 (in Russian).
12. Kobayashi H, Higashiura Y, Shigetomi H, Kajihara H. Pathogenesis of endometriosis: The role of initial infection and subsequent sterile inflammation (Review). Mol Med Rep 2014; 9: 9–15. https://doi.org/10.3892/mmr.2013.1755
13. Invitti AL, Schor E, Parreira RM et al. Inflammatory cytokine profile of co cultivated primary cells from the endometrium of women with and without endometriosis. Mol Med Rep 2018; 18: 1287–96.
14. Durmus AB, Cengiz SD, Yilmaz H et al. The levels of matrix metalloproteinase-9 and neutrophil gelatinase-associated lipocalin in different stages of endometriosis. J Obstetrics Gynaecol 2019; 39 (7): 991–5. DOI: 10.1080/01443615.2019.1584889
15. Ferreira EM, Giorgi VSI, Rodrigues JK et al. Systemic oxidative stress in the early follicular phase as a possible mechanism underlying the pathogenesis of mild endometriosis-related infertility and a helpful tool to predict ICSI outcomes: a pilot study. Reprod BioMed Online 2019; 39 (5): 785–94. DOI: https://doi.org/10.1016/j.rbmo.2019.06.011
16. Nisenblat V, Bossuyt P, Shaikh R et al. Blood biomarkers for the non-invasive diagnosis of endometriosis (Review). Cochrane Database Syst Rev 2016; 5: CD012179.
17. González-Foruria I, Santulli P, Chouzenoux S et al. Dysregulation of the ADAM17/Notch signalling pathways in endometriosis: from oxidative stress to fibrosis. Mol Human Reprod 2017; 23 (7): 488–99.
18. Kavian N, Servettaz A, Mongaret C et al. Targeting ADAM-17/notch signaling abrogates the development of systemic sclerosis in a murine model. Arthritis Rheum 2010: 62 (11): 3477–87.
19. Sua R-W, Struga MR, Jeonga J-W et al. Aberrant activation of canonical Notch1 signaling in the mouse uterus decreases progesterone receptor by hypermethylation and leads to infertility. Proc Natl Acad Sci 2016; 113 (8): 2300–5.
20. Su RW, Strug MR, Joshi NR et al. Decreased Notch pathway signaling in the endometrium of women with endometriosis impairs decidualization. J Clin Endocrinol Metab 2015; 100 (3): E433–E442.
21. Bulun SE, Cheng YH, Yin P et al. Progesterone resistance in endometriosis: link to failure to metabolize estradiol. Mol Cell Endocrinol 2006; 248: 94–103.
22. Chae U, Min JY, Kim SH et al. Decreased Progesterone Receptor B/A Ratio in Endometrial Cells by Tumor Necrosis Factor-Alpha and Peritoneal Fluid from Patients with Endometriosis. Yonsei Med J 2016; 57 (6): 1468–74.
23. Bulun SE, Monsavais D, Pavone ME et al. Role of estrogen receptor-beta in endometriosis. Semin Reprod Med 2012; 30: 39–45.
24. Lessey BA, Lebovic DI, Taylor RN. Eutopic endometrium in women with endometriosis: ground zero for the study of implantation defects. Semin Reprod Med 2013; 31: 109–24.
25. Liao T, Lee Y-C, Tzeng C-R et al. Mitochondrial translocation of estrogen receptor-b affords resistance to oxidative insult-induced apoptosis and contributes to the pathogenesis of endometriosis. Free Radic Biol Med 2019; 134: 359–73.
26. Nisenblat V, Prentice L, Bossuyt P et al. Combination of the non-invasive tests for the diagnosis of endometriosis (Review). Cochrane Database Syst Rev 2016; 7: CD012281.
Авторы
А.С. Сафронова, М.Ю. Высоких, В.Д. Чупрынин, Н.А. Буралкина*
ФГБУ «Национальный медицинский исследовательский центр акушерства, гинекологии и перинатологии
им. акад. В.И. Кулакова» Минздрава России, Москва, Россия
*natalyaburalkina@yandex.ru
Kulakov National Medical Research Center for Obstetrics, Gynecology and Perinatology, Moscow, Russia
*natalyaburalkina@yandex.ru
ФГБУ «Национальный медицинский исследовательский центр акушерства, гинекологии и перинатологии
им. акад. В.И. Кулакова» Минздрава России, Москва, Россия
*natalyaburalkina@yandex.ru
________________________________________________
Kulakov National Medical Research Center for Obstetrics, Gynecology and Perinatology, Moscow, Russia
*natalyaburalkina@yandex.ru
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