Adenomyosis is a benign uterine pathology characterized by the presence of ectopic endometrium (EkEA), i.e., endometrium located in an uncharacteristic site, within the uterine myometrium. The disease has not yet been sufficiently researched to fully understand its etiology, and likewise, an effective method of treatment has not yet been developed. The aim of the thesis was to collect molecular data on eutopic (EvEA) – i.e., located in its proper site – and ectopic endometrium in adenomyosis and the associated myometrium, to systematically categorize them according to the pathophysiological mechanisms of the disease and thereby present some possible causes of the condition. Molecular data analysis from the literature showed that adenomyosis is characterized by increased local production of estradiol and uterine hyperperistalsis, accompanied by elevated expression of oxytocin receptors and changes in ion channel expression, which together also mark the beginning of an important process known as TIAR (tissue injury and repair). Another key process is EMT (epithelial to mesenchymal transition), during which epithelial cells lose their specific biomarkers and acquire mesenchymal ones, along with loss of apical-basal polarity, increased migration, and invasiveness of the endometrium; this process is further facilitated by changes in the organization of the extracellular matrix. Crucial to lesion survival and formation are also excessive angiogenesis, accompanied by increased expression of certain angiogenic factors, the formation of new nerve fibers with overly expressed neurogenic factors, excessive cellular proliferation, and inhibited apoptosis. Finally, indispensable are the immunological changes, which include immune cell accumulation, insufficient immune surveillance, and altered expression of inflammatory mediators.
|
