Endometriosis: Update of Pathophysiology, (Epi) Genetic and Environmental Involvement

• Published in: Biomedicines Vol. 11; no. 3; p. 978
• Main Authors: Monnin, Nicolas, Fattet, Anne Julie, Koscinski, Isabelle
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 01.03.2023; MDPI
• Subjects: 17β-Estradiol; Apoptosis; Aromatase; Bisphenol A; Cell growth; Chronic pain; Cloning; Demethylation; Dioxins; endocrine disruptor; Endocrine disruptors; Endometriosis; Endometrium; Environmental factors; Enzymes; epigenetics; Estrogen receptors; Estrogens; Fallopian tubes; Fertility; Gynecology; Heat shock proteins; Infertility; Inflammation; Kinases; Menstruation; molecular pathophysiology; Mutation; Ovaries; Pathophysiology; Physiological aspects; Prenatal experience; Progenitor cells; Progesterone; Reproductive system; Review; Tumorigenesis; United States; endometriosis; endocrine disruptor; molecular pathophysiology; epigenetics
• ISSN: 2227-9059; 2227-9059
• DOI: 10.3390/biomedicines11030978

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.