Modern Knowledge of the Pathogenetic Mechanisms of Pulmonary Fibrosis Formation

A. S. Shapovalova
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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
肺纤维化形成的病理机制的现代知识
本研究的目的是分析现代文献资料对肺纤维化形成的发病机制的看法。材料和方法。研究中采用了分析方法和文献语义学方法。在科学检索过程中,对现代国内外文献的39个来源进行了回顾和分析。结果和讨论。肺纤维化是一种异质性的慢性、进行性和不可治愈的肺间质性疾病,其特征是疤痕形成和肺实质的不可逆破坏,并伴有病理改变区域的弹性和气体交换障碍。肺纤维化的发生机制是由其根本原因决定的。肺纤维化有三种不同的病理类型:普通间质性肺炎、纤维化性非特异性间质性肺炎和气道纤维化。它们的形态学差异是基于纤维化的分布(弥漫性或点状)和解剖位置。肺纤维化的发展在大多数情况下是由于先前由各种病因引起的肺部急性炎症的结果,在不及时开始或错误选择治疗的情况下,导致肺部纤维组织沉积。人们认为,肺纤维化的出现和随后的进展可归因于肺泡上皮细胞在各种刺激(包括损伤)下反复损伤后的修复过程。肺泡上皮细胞功能丧失或数量减少可导致肺实质修复不当,从而导致纤维化。肺泡上皮细胞受损时可释放多种细胞因子,如转化生长因子-β1、肿瘤坏死因子-α、血小板源性生长因子等。这些细胞因子可以促进成纤维细胞的积累。除了细胞因子反应外,肺对损伤的反应还包括肌成纤维细胞的刺激,当肌成纤维细胞被激活时,它可以作为主要的胶原生成细胞。这导致胶原蛋白的大量沉积,并随后影响肺组织的正常结构和功能。结论。肺纤维化是一种进行性肺部疾病,可导致肺组织的形态功能重构。在工作过程中,分析了三种肺纤维化发展模式的存在。尽管研究历史悠久,科学文献对这一问题的报道也很好,但目前对肺纤维化形成的机制研究还不够充分
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