Сучасні відомості про патогенетичні механізми формування пневмосклерозу

Abstract

The purpose of the study was to analyze literary sources on the study of modern views on information about the pathogenetic mechanisms of the formation of pulmonary fibrosis. Materials and methods. Analytical and bibliosemantic methods were used in the research. During the scientific search, 39 sources of modern domestic and foreign literature were reviewed and analyzed. Results and discussion. Pulmonary fibrosis is a heterogeneous group of chronic, progressive and incurable interstitial lung diseases characterized by scar formation and irreversible destruction of the lung parenchyma and is accompanied by disorders of elasticity and gas exchange in pathologically altered areas. The mechanism of development of pulmonary fibrosis is determined by its root causes. There are three distinct pathologic patterns of pulmonary fibrosis: usual interstitial pneumonia, fibrotic nonspecific interstitial pneumonia, and airway fibrosis. Their morphological differences are based on the distribution of fibrosis (diffuse or spotty) and anatomical location. The development of pulmonary fibrosis in most cases is a consequence of a previous acute inflammation of the lungs caused by various etiological factors, which in the case of untimely started or incorrectly selected treatment causes the deposition of fibrous tissue in the lungs. It is believed that the appearance and subsequent progression of pulmonary fibrosis can be attributed to reparative processes after repeated injuries of alveolar epithelial cells in response to various stimuli, including injuries. Loss of function or reduction in the number of alveolar epithelial cells can lead to improper repair of the lung parenchyma, which can lead to fibrosis. Various cytokines such as transforming growth factor-β1, tumor necrosis factor-α, and platelet-derived growth factor can be released when alveolar epithelial cells are damaged. These cytokines can promote the accumulation of fibroblasts. In addition to the cytokine response, the lung’s response to injury includes the stimulation of myofibroblasts, which when activated serve as the primary collagen-producing cell. This leads to massive deposition of collagen and subsequently affects the normal structure and function of lung tissue. Conclusion. Pulmonary fibrosis is a progressive lung disease that leads to morpho-functional restructuring of lung tissue. In the course of the work, the presence of three models of the development of pulmonary fibrosis were analyzed. Despite the long history of study and good coverage of the problem in the scientific literature, currently the mechanisms of formation of pulmonary fibrosis remain insufficiently studied