Endometriosis is a chronic disease caused by ectopic endometrial tissue. Endometriotic implants induce inflammation, leading to chronic pain and impaired fertility. Characterized by their dependence on estradiol (via estrogen receptor β (ESRβ)) and their resistance to progesterone, endometriotic implants produce their own source of estradiol through active aromatase. Steroidogenic factor-1 (SF1) is a key transcription factor that promotes aromatase synthesis. The expression of and is enhanced by the demethylation of their promoter in progenitor cells of the female reproductive system. High local concentrations of estrogen are involved in the chronic inflammatory environment favoring the implantation and development of endometriotic implants. Similar local conditions can promote, directly and indirectly, the appearance and development of genital cancer. Recently, certain components of the microbiota have been identified as potentially promoting a high level of estrogen in the blood. Many environmental factors are also suspected of increasing the estrogen concentration, especially prenatal exposure to estrogen-like endocrine disruptors such as DES and bisphenol A. Phthalates are also suspected of promoting endometriosis but throughmeans other than binding to estradiol receptors. The impact of dioxin or tobacco seems to be more controversial.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10046867 | PMC |
| http://dx.doi.org/10.3390/biomedicines11030978 | DOI Listing |
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Recent Trends in Medical Management of Endometriosis.
J Obstet Gynaecol India
December 2024
Nowrosjee Wadia Maternity Hospital, Mumbai, India.
Endometriosis affects about 10 percent women in the reproductive age group globally and approximately 42 million in India. Managing the patient's pain symptoms associated with endometriosis appears to be the cornerstone in endometriosis disease management. The ideal medical treatment in endometriosis would be suppressing estradiol enough to alleviate symptoms of endometriosis but maintain sufficient levels to mitigate hypoestrogenic side effects.
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Department of Obstetrics & Gynaecology, The Chinese University of Hong Kong, Hong Kong, China.
As a chronic gynecological disease, endometriosis is defined as the implantation of endometrial glands as well as stroma outside the uterine cavity. Proliferation is a major pathophysiology in endometriosis. Previous studies demonstrated a hormone named melatonin, which is mainly produced by the pineal gland, exerts a therapeutic impact on endometriosis.
View Article and Find Full Text PDFLaparoscopic surgery for left ovarian hemorrhage in a patient with an implantable left ventricular assist device on antithrombotic therapy and a history of right salpingo-oophorectomy open surgery for right ovarian bleeding: A case report.
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Osaka University Graduate School of Medicine, Department of Obstetrics and Gynecology, 2-2, Yamada-oka, Suita City, 565-0871 Osaka, Japan.
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View Article and Find Full Text PDFReceptive window might be shorter in patients with endometriosis and lesions cyclically prepare for implantation.
F S Sci
December 2024
Implantation and Pregnancy Research Laboratory, School of Health and Biomedical Sciences, RMIT University, Bundoora, Victoria, Australia. Electronic address:
Objective: To investigate whether endometrial receptivity is affected in patients with endometriosis using podocalyxin (PCX) as a functional biomarker and to study how endometriotic lesions display PCX and the potential pathological implications.
Design: We have previously reported that PCX, an anti-adhesion glycoprotein and barrier protector, is dynamically regulated in the endometrium and acts as a key negative regulator of epithelial receptivity. Early in the cycle both luminal epithelium (LE, lining the endometrial surface) and glandular epithelium (GE, residing within the tissue) strongly express PCX, but in the receptive window, PCX is selectively downregulated in LE, switching the endometrial surface to an adhesive state for embryo attachment/implantation; meanwhile, PCX expression is maintained in GE until postreceptivity.
Extracellular vesicle-packaged PKM2 from endometriotic stromal cells promotes endometrial collagen I deposition by inhibiting autophagy in endometriosis.
Cell Signal
November 2024
Center for Reproductive Medicine and Obstetrics and Gynecology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, China. Electronic address:
Article Synopsis
- Aberrant collagen I deposition in the endometrium during the implantation window negatively affects decidualization in endometriosis patients, potentially lowering their chances of pregnancy through IVF.
- The study identified that mid-secretory phase endometrial tissue from endometriosis patients showed increased collagen I along with decreased autophagy in endometrial stromal cells (ESCs), which is crucial for collagen degradation.
- Extracellular vesicles from ectopic ESCs were found to carry elevated levels of PKM2, which inhibited ESC autophagy and increased collagen I deposition via the Akt/mTOR signaling pathway, presenting a possible target for enhancing IVF success rates in endometriosis patients.
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