MORPHOFUNCTIONAL STATE OF THE ENDOTHELIAL SYSTEM IN WORKERS OF THE KUZBASS COAL INDUSTRY
The professional dust pathology of the respiratory organs in Kuzbass remains relevant due to its high prevalence among coal workers. When entering the body, the components of coal cause the development of pneumoconiotic fibrosis. Innovative ideas about fibrosis morphogenesis in recent years have shifted to the molecular level and appeal to the state of cellular receptors, the expression of some genes and the repression of others, a cardinal change in the cellular phenotype, which is the platform on which complex pathological processes occur. The purpose of the study is to study the pathomorphological changes in the endothelial system of coal miners with various years of underground work. Materials and methods. Histological, morphometric and immunohistochemical studies of the hemodynamic system obtained during 50 autopsy works of a group of Kuzbass miners working in underground conditions were carried out. Arteries and veins of small and large circulation, vessels of microcirculatory bed of internal organs were studied. Immunohistochemical testing was performed using monoclonal antibodies (proliferation marker Ki-67; oncogene of proapoptotic activity Bcl-2; endothelial function factors CD-31 and CD-34). Results. In the coal industry, there are pronounced changes in the vessels of internal organs, which manifest themselves in the potomorphological changes of endothelial cells. These pathological changes cause «vascular obstruction» which, along with fibroplastic changes and macrophage inflammation, contribute to the development of hypoxia, while being the main mechanism for the development of multi-organ pathology. The main source of fibrosis in the lung is activated myofibroblasts, the precursors of which can be as resident fibroblast-like cells. The source may be dedifferentiated epithelial cells including endothelial cells. Conclusions. Perceptions of endothelial dysfunction are only one facet of epithelial-mesenchymal transformation as a mechanism of major pathological changes in pneumoconiosis should serve as a foundation for further in-depth study and understanding of the complex pathogenetic aspects of this problem in medicine.