Cellular and molecular basis for endometriosis-associated infertility

Abstract

Endometriosis is a gynecological disease characterized by the presence of endometrial glandular epithelial and stromal cells growing in the extra-uterine environment. The disease afflicts 10%–15% of menstruating women causing debilitating pain and infertility. Endometriosis appears to affect every part of a woman’s reproductive system including ovarian function, oocyte quality, embryo development and implantation, uterine function and the endocrine system choreographing the reproductive process and results in infertility or spontaneous pregnancy loss. Current treatments are laden with menopausal-like side effects and many cause cessation or chemical alteration of the reproductive cycle, neither of which is conducive to achieving a pregnancy. However, despite the prevalence, physical and psychological tolls and health care costs, a cure for endometriosis has not yet been found. We hypothesize that endometriosis causes infertility via multifaceted mechanisms that are intricately interwoven thereby contributing to our lack of understanding of this disease process. Identifying and understanding the cellular and molecular mechanisms responsible for endometriosis-associated infertility might help unravel the confounding multiplicities of infertility and provide insights into novel therapeutic approaches and potentially curative treatments for endometriosis.

Intrafollicular interleukin-8, interleukin-12, and adrenomedullin are the promising prognostic markers of oocyte and embryo quality in women with endometriosis

“…An exhaustive meta-analysis suggests that patients with endometriosis-associated infertility undergoing in vitro fertilization (IVF) have a decreased pregnancy rate as compared with other indications for IVF [2]. The data also suggest that endometriosis affects both the development of the oocyte and embryo and the receptivity of the endometrium [3].…”

Elevated Peritoneal Fluid TNF-α Incites Ovarian Early Growth Response Factor 1 Expression and Downstream Protease Mediators: A Correlation With Ovulatory Dysfunction in Endometriosis

“…1 The presence of endometriotic lesions in the peritoneal cavity is commonly associated with pain and subfertility, yet mechanisms causing these conditions in endometriosis are diverse and not well characterized. [1][2][3][4][5][6] Pituitary-ovarian dysfunction manifested as abnormal patterns of luteinizing hormone (LH) secretion including a delayed and reduced amplitude LH surge and LH receptor (LHR) disorder contribute to infertility in women with endometriosis. 3,[7][8][9][10][11] Reduced circulating estradiol concentrations during the preovulatory phase, reduced estradiol and progesterone during the early luteal phase and anomalous estrogen receptor, progesterone receptor and progesterone resistance have also been described.…”

Study of endometriosis in women of reproductive age, laparoscopic management and its outcome

“…These altered peritoneal fluid composition and adhesions cause severe tubal dysfunction, 9 the actual prevalence is difficult to quantify because of its very wide range in various studies across the world. [10][11][12] In one of the studies, it has been shown that approximately 47% of women with infertility have endometriosis. 13 In a study done by Tsuzi et al, the prevalence was 63%.…”