GLI1 is increased in ovarian endometriosis and regulates migration, invasion and proliferation of human endometrial stromal cells in endometriosis

Endometriosis, a common gynecological benign disorder, is classically characterized by the presence of endometrial-like tissue outside of the uterine cavity, primarily the pelvic peritoneum, ovaries, and rectovaginal septum (1). Affecting 10–15% of female population of reproductive age, the stigmata of endometriosis include dysmenorrhea, dyspareunia, chronic pelvic pain and infertility (2). The formation of a lesion depends on the survival, attachment, growth, neo-angiogenesis, and invasion of the endometrial cells at the ectopic sites (3,4). Despite many years of research, until now, the etiology and pathogenesis of endometriosis remains poorly understood. Moreover, an effective strategy to prevent and control the endometriosis development is still lacking. Therefore, the underlying molecular and cellular mechanisms linking the pathogenesis of endometriosis need to be unraveled that could be further manipulated to explore new effective approaches for endometriosis therapy