Bridging the preclinical gap: new models of endometriosis for disease and drug discovery

Endometriosis is an oestrogen-dependent condition that affects an estimated 190 million women worldwide [1]. Endometrial-like lesions form outside of the uterus and often invade adjacent organs such as the ovaries, bowel and peritoneal wall. Similar to the uterine lining, these lesions expand and bleed under hormonal regulation. Inflammation contributes to the development of scar tissue and adhesions. Limited understanding of disease pathophysiology adds to the delays in diagnosis and compromised quality of life. Whilst endometriosis can be asymptomatic, for others it is debilitating with symptoms of chronic pelvic pain, dyspareunia, fatigue and infertility. In severe cases, complications such as ureteric strictures and bowel obstruction may arise. Associated loss of work and healthcare costs, estimated at £8.2bn a year, have a significant impact on the UK economy [2].
No current treatment options attenuate both pain and lesion growth without affecting fertility. Management often involves a combination of painkillers, hormone treatment that suppresses ovarian function and/ or surgical excision of lesions. Even after surgery, over 50 percent of patients require reoperation due to the regrowth of endometriosis lesions or paradoxically through surgically-induced fibrosis [3].
One major challenge to the development of effective treatment strategies is the lack of advanced 3D human co-culture models of endometriosis that recapitulate different lesion subtypes and are amenable to manipulation [4]. Addressing this gap is vital to bridge the chasm between scientific discovery and human application for this significant unmet clinical need.