Abstract
Endometriosis is a female reproductive disorder characterized by growth of uterine cells and tissue in distant sites. Around 2–10% of women experience this condition during reproductive age, 35–50% of whom encounter fertility issues or pain. To date, there are no established methods for its early diagnosis and treatment, other than surgical procedures and scans. It is difficult to identify the disease at its onset, unless symptoms such as infertility and/or pain are present. Determining the mechanisms involved in its pathogenesis is vital, not only to pave the way for early identification, but also for disease management and development of less invasive but successful treatment strategies. Endometriosis is characterized by cell proliferation, propagation, evasion of immunosurveillance, and invasive metastasis. This review reports the underlying mechanisms that are individually or collectively responsible for disease establishment and evolution. Treatment of endometriosis mainly involves hormone therapies, which may be undesirable or have their own repercussions. It is therefore important to devise alternative strategies that are both effective and cause fewer side effects. Use of phytochemicals may be one of them. This review focuses on pharmacological inhibitors that can be therapeutically investigated in terms of their effects on signaling pathways and/or mechanisms involved in the pathogenesis of endometriosis.
Highlights
There is an abundance of articles reporting multifactorial causes for the onset of endometriosis, as the pathogenesis of this disease appears to include a range of features, including ectopic endometrial tissue, altered immunity, unbalanced cell proliferation and apoptosis, aberrant endocrine signaling, and genetic factors [5]
NF-κB-activated macrophages release proinflammatory cytokines and growth factors involved in boosting inducible nitric oxide synthase, cyclooxygenase-2 (COX-2), IL-1, IL-6, interleukin 8 (IL-8), tumor necrosis factor alpha (TNF-α), and vascular endothelial growth factor (VEGF)
A number of reports have found that women with endometriosis demonstrate increased expression and release of various proinflammatory cytokines and growth factors—such as IL-1, IL-6, IL-8, epidermal growth factor, and hepatocyte growth factor—in their ectopic and eutopic endometrium and their peritoneal fluid [17,18,27,28]
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Endometriosis is becoming increasingly common but remains a perplexing disease It is an estrogen-dependent disorder defined by the presence of endometrium-like tissue in any extrauterine site, even those distant to the uterus, including the pelvic peritoneum, ovaries, and bowel and, rarely, extrapelvic locations [1,2,3]. There is an abundance of articles reporting multifactorial causes for the onset of endometriosis, as the pathogenesis of this disease appears to include a range of features, including ectopic endometrial tissue, altered immunity, unbalanced cell proliferation and apoptosis, aberrant endocrine signaling, and genetic factors [5] For this reason, a very thorough and comprehensive understanding is needed to detect and investigate the physiological, cytological, and immunological events that take place in the microenvironment of the uterus in order to characterize the origins and evolution of the disease. We will explore how these mechanisms and specific molecules can be used to develop novel therapeutic options against endometriosis
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