Endometriosis is a dyshormonal immune-dependent genetically determined disease, which appears as an endometrioid tissue that grows outside the uterine. Endometriosis is one of the most urgent problems of medicine. To date, new concepts of the endometriosis etiology and pathogenesis have been developed, but, despite their abundance, there is no unified theory. Genetic and epigenetic factors result in changes in an expression of aromatase, steroidogenic factor 1, and estrogen receptors are suggested to be the main cause of endometriosis. These changes lead to an active synthesis of various pro-inflammatory agents and a nerve growth factor, that are important in the development of pain syndrome. Also, changes in the progesterone receptor functioning and the local progesterone resistance development decrease the antiproliferative activity, apoptosis, and the anti-inflammatory substances level, as well as increase the prostaglandin, metalloproteinase activity, and level of hypoxia factors. In addition, there are shreds of evidence that endometriosis is associated with the risk of malignant tumors development, so new concepts for understanding these mechanisms are actively developing. Some of these mechanisms are discussed in this review.
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