Abstract
Background: The complexity of endometriosis pathophysiology, the diversity of disease phenotypes, and the fact that the disease only occurs in menstruating primates have limited the pace of progress in our understanding of this very common and sometimes debilitating disease. Despite the difficulties investigators face, it has been clearly established that complex mechanisms involving steroid hormones, their metabolism, and their receptors are fundamentally important in the establishment and progression of endometriosis lesions.
Objective: We have attempted to review the extant knowledge about the roles of steroid hormones on endometriosis pathogenesis and pathophysiology in the hope that such a review will be useful for scientists and clinicians seeking to better understand, diagnose, and treat this disease.
Results: Eutopic endometrium and ectopic lesions from women with endometriosis can produce estrogen locally. Further, the expressions of steroid hormone receptors and enzymes are significantly altered in these tissues. Together, these changes alter steroid signaling for embryo implantation and enhance the potential for lesion establishment, maintenance, and growth. Several hormonal lines of treatment have proven to be effective in reducing symptoms of endometriosis.
Conclusion: Sex-steroids play a dominant role in endometriosis pathophysiology. Targeting sexsteroid anabolism, catabolism, and action is clinically important, and an understanding of these mechanisms is essential to developing more precise therapies.
Keywords: Endometriosis, ERβ, ERα, PR, aromatase, 17 beta hydroxysteroid dehydrogenase, steroid sulfatase.
Graphical Abstract
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