Данная работа посвящена клеточной популяции макрофагов в качестве одной из наиболее значимых структур контроля и управления гомеостазом ткани эндометрия, где данные клетки координируют работу клеточных популяций, составляющих коммуникационную систему. Посредством возможности поляризации своего фенотипа макрофаги способны выполнять множество функций, регулируя структурные преобразования эндометрия в зависимости от фазы цикла или возникновения патологии. Высокая концентрация эстрогена в фолликулярную фазу является сигналом для макрофагов эндометрия к запуску целого ряда событий, затрагивающих все остальные клеточные популяции, в том числе и мезенхимальные стволовые клетки эндометрия. Данные взаимодействия приводят к активации пролиферации фибробластоподобных клеток с последующим их созреванием, а также ангиогенезу и нейрогенезу, что составляет стромальный компонент функционального слоя эндометрия. Особый интерес представляет влияние макрофагов на восполнение железистого компонента функционального слоя эндометрия в процессе железистого ремоделирования, в основе которого лежит эпителиально-мезенхимальный переход. В фазу секреции макрофаги эндометрия координируют создание клеточного микроокружения для обеспечения толерантности клеток иммунной системы матери к антигенам плода, а также поддержание гомеостаза и роста плаценты. При отсутствии оплодотворения макрофаги активно способствуют разрушению основного вещества ткани эндометрия, что обеспечивает менструальный распад в фазу десквамации. Рассмотрена роль функциональной разбалансировки макрофагов как патогенетического звена целого ряда патологий эндометрия и беременности. Таким образом, показана центральная роль макрофагальной популяции в управлении коммуникационной системой ткани эндометрия. Понимание данных аспектов открывает новые возможности управления менструальным циклом, планированием и сохранением беременности.

Endometriosis nowadays still a disease with an undisclosed pathogenesis. This article demonstrates and explains the possibility of different variants of dissemination of endometrioid cells in the body with the formation of foci of extragenital endometriosis in organs and tissues remote from the pelvis, complementing and confirming the theory of utero-peritoneal reflux in the development of endometriosis as the most reasonable. Endometrioid heterotopias have a more developed lymphatic network compared to the normal endometrium due to active lymphangiogenesis, and, having a tendency to invasive growth, endometrioid heterotopia is a source of endometrioid cells spreading along the direction of lymph outflow from the most typical locations (pelvic organs) with damage to the inguinal and pelvic lymph nodes. Lymphatic dissemination in adenomyosis is observed in every fourth patient, which requires revision of the surgery protocol with excision of regional lymph nodes to prevent relapses. The presence of cases of pulmonary endometriosis and endometrioid liver cysts makes hematogenic dissemination of endometriosis from the primary source in the pelvic region obvious. The most frequent localizations of endometrioid heterotopias are located near the corresponding venous plexuses of the small pelvis, the outflow from which occurs mainly through the inferior vena cava, without anatomical obstacles for hematogenic dissemination of endometrioid cells with subsequent lung damage. For liver involment, it is likely that endometriosis in the distal parts of the colon is important, the venous outflow from which is directed to the portal vein system. Endometriosis of the diaphragm – is an example transcoelomic spread with predominant location on the right dome of the diaphragm, as the right subphrenic space communicates with the pelvic cavity through the right lateral channel, which justifies the possibility of such involments of the diaphragme in context of the theory of uteroperitoneal reflux.Thus, the theory of menstrual regurgitation and the theory of hemato-lymphatic dissemination are components of a single pathogenetic model of the distribution of endometrioid cells in the body.

This article summarizes the results of the most recent studies exploring changes in the stromal component of the endometrial tissue during malignant transformation in patients with precancerous conditions, particularly transformation of glandular hyperplasia of the endometrium into endometrioid adenocarcinoma. We cover the most important issues related to microcirculatory remodeling and changes in the cellular microenvironment of the stroma in terms of the effects exerted by biologically active molecules produced by different cell populations. We analyzed specific changes occurring in the stromal components in various types of glandular hyperplasia of the endometrium and changes during endometrioid adenocarcinoma progression. We focus on the prognostic and diagnostic values of these morphological changes, considering the results of the latest molecular studies, which can be later used for personalization of patient prognosis.

Cardiac lymphatic vessels play a vital role in maintaining homeostasis in both physiological and pathological conditions, providing outflow of metabolites. It has been shown that myocardial infarction and postinfarction cardiac remodeling is accompanied by the lymphatic remodeling, which entails functional disorders and is of great importance in heart failure pathogenesis. As a result of progressive myocardial edema, hypoxia and fibrosis of the interstitial space increase, aggravating edema. Other pathways of additional myocardial damage and contractility reduction are triggered. Lymphatic efflux is associated with arrhythmias. Experimental models showed the positive effect of exogenous activation of lymphangiogenesis in relation to the prevention and treatment of heart failure, which can be further used to improve treatment regimens. This review discusses cardiac lymphatic remodeling after myocardial infarction, as well as the pathogenesis of related complications.

Reticuloendothelial system (RES) is considered one of the local immune response regulation centers. It takes part in most physiological and pathological processes, namely, in local homeostasis, in regulation of trophism and immunological responses of both primary and secondary immune responses. The main cell population of (RES) is a macrophage, which is a stationary cell that can move only within the tissue layer. Dendritic cells as representatives of (RES) as well are under direct control of macrophages. Up to 80% of all immunocompetent cells are concentrated in the intestinal mucosa. For adequate interaction with the intestinal microbiota and ensuring immunological tolerance to normal commensals, there is a lymphoid tissue associated with the intestinal mucosa (gut-associated lymphoid tissue – GALT), in which mononuclear phagocytes perform their most significant functions. When pathogenic microorganisms enter the mucosa, the network of resident macrophages as an immune barrier triggers an inflammatory response to further stabilize homeostasis. However, a pronounced microbial and antigenic load in the gut requires the mandatory presence of specific immune cells – lymphocytes, whose immature forms are located in GALT structures and specialize under the guidance of mononuclear phagocytes. After the final differentiation, lymphocytes expressing integrin α4β7 are able to return from the systemic bloodstream to the intestinal mucosa to perform highly specific functions. This phenomenon is called the homing effect. It was noted that in non-specific ulcerative colitis and Crohn's disease, both the number of regulatory T-lymphocytes and their expression of integrin α4β7 increases. The pathology of the homing effect, according to some researchers, explains the possibility of follow-up secondary lesions in chronic inflammatory bowel diseases with the development of systemic pathology.