Mitochondrial Dysfunction in Endometriosis

What is Endometriosis?

Endometrial tissue is usually restricted to the uterus. In endometriosis, however, endometrial tissue can grow in locations, including the ovaries and fallopian tubes, as well as in nearby and more distant tissue (bladder, rectum, etc). Consequently, endometrial tissue in these other areas can result in inflammation and scarring. Pelvic pain is usually the main
presenting symptom; being chronic in 50% of patients, with 70% experiencing pelvic pain during menstruation even during ovulation.

Infertility is common, being evident in approximately 50% of people presenting with endometriosis. Between 10% of western women and about 15% of Asian women will experience endometriosis, most typically with a first presentation at 30-40 years, often as a consequence of difficulties in conceiving.

Factors linked to endometriosis pathophysiology include: increased oxidative and nitrosative stress (O&NS), chronic immune inflammation, increased immune tolerance, autoimmunity, t helper (Th)17 cells and interleukin (IL)-17. Estrogen at the estrogen receptor-alpha (ERα) can exacerbate symptoms, with estrogen also having regulatory, symptomatic, effects via the ERβ. As both of these estrogen receptors can be mitochondria-located, there can be significant changes in mitochondria functioning in endometriosis.

As such, endometriosis shows alterations in mitochondrial functioning, oxidative stress regulation and increased trophic factors, linking endometriosis with tumor-associated pathophysiology, meaning it is viewed as a benign cancer.

Endometriosis, like a growing number of other medical conditions, shows alterations in the gut microbiome, especially via a decrease in the short-chain fatty acid (SCFA), butyrate.