Endometriosis, a leading cause of infertility, is characterized by the presence of endometrial-like tissue outside the uterus, which results in anatomical distortions, adhesions, fibrosis, as well as hormonal and immune system disruptions. This condition is increasingly recognized as a complex interplay of multiple mechanisms that hinder fertility. Recent studies provide further insights into how these factors contribute to infertility in individuals with endometriosis.
One of the primary mechanisms is the alteration of the hypothalamic-pituitary-ovarian axis, which affects the secretion of gonadotropins and steroid hormones. This dysregulation impairs ovulation and disrupts the conditions necessary for embryo implantation, ultimately leading to fertility decline. In addition, changes in the hypothalamic-pituitary-adrenal axis result in elevated levels of cortisol and prolactin. These hormonal disturbances contribute to the stress-related symptoms, such as depression and anxiety, commonly observed in individuals with endometriosis.
The immune system also plays a significant role in endometriosis-related infertility. Abnormal interactions between endometrial cells and immune cells can lead to changes in the local tissue microenvironment, fostering inflammation and epithelial-mesenchymal transition. This creates an environment unfavorable for successful embryo implantation. Epithelial cells, stromal cells, and immune cells within the affected tissue release an array of cytokines, chemokines, and autoantibodies, all of which contribute to the inflammatory response and hinder reproductive processes.
Furthermore, oxidative stress is recognized as another key factor in endometriosis-related infertility. This condition adversely impacts ovarian reserve and embryo development. A disrupted redox balance, impaired mitochondrial function, and dysregulated lipid metabolism generate a pro-oxidative environment, which diminishes oocyte quality and reduces sperm and embryo viability. Iron-induced oxidative stress exacerbates these effects, leading to a negative impact on fertility outcomes.
Together, these findings underscore the multifaceted nature of endometriosis-related infertility. Advancements in understanding the underlying mechanisms of this condition hold promise for the development of more effective strategies to manage and treat infertility in affected individuals.
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