Endometriosis and Epigenetics: What do we Know?
Endometriosis is a condition where endometrial glands and endometrial stroma are present outside the uterus. It is common with prevalence between 10 and 15% in females of reproductive
age, especially between the ages of 30 and 40. However, it can also affect prepubertal, pubertal and postmenopausal women. Endometriosis is classified as a benign inflammatory process that may be
asymptomatic or may cause a variety of symptoms, ranging from chronic vague pelvic pain to dysmenorrhea, menorrhagia, dyspareunia, dyschezia, and dysuria, etc.
According to Sampson, viable endometrial tissue fragments are spread from the uterine cavity to the fallopian tubes and then to the peritoneal cavity, by a gradient of pressure due to the dyssynergic contractions of the uterus. In the peritoneal cavity, these fragments may implant and grow with the hormonal changes.
This concept suggests that the coelomic epithelium, which is the embryologic precursor of both peritoneal and endometrial tissues, undergo a metaplastic transformation from peritoneal cells to endometrial-like tissue. Hormonal, biochemical and/or immunological factors may be the origin of this metaplasia.
Methylation of the 5-carbon position of the pyrimidine ring of cytosines, paired with a complimentary guanosine (CpG sites) creates CpG islands in gene promoters. This modification
leads to transcription suppression causing silencing of the corresponding gene. This process of methylation is stable, yet reversible.
In fact, DNA coding for proteins such as CYP19 (aromatase cytochrome P450) and steroidogenic acute regulatory protein (StAR) and for nuclear receptors such as estrogen receptor-β (ER-β) and steroidogenic factor-1 (SF-1) are hypomethylated in endometriosis. This process leads to an increased 17β-estradiol biosynthesis.
Women Health Open J. 2018; 4(1): 1-7. doi: 10.17140/WHOJ-4-125
