Pathogenesis of pulmonary fibrosis

• Published in: Arkhiv patologii Vol. 86; no. 4; p. 58
• Main Authors: Rybakova, M G, Myurzep, A E
• Format: Journal Article
• Language: English; Russian
• Published: Russia (Federation) 2024
• Subjects: COVID-19 - complications; COVID-19 - pathology; Cytokines - metabolism; Fibroblasts - metabolism; Fibroblasts - pathology; Humans; Myofibroblasts - metabolism; Myofibroblasts - pathology; Pulmonary Fibrosis - etiology; Pulmonary Fibrosis - metabolism; Pulmonary Fibrosis - pathology; Renin-Angiotensin System; SARS-CoV-2; COVID-19; post-COVID syndrome; pulmonary fibrosis
• ISSN: 0004-1955
• DOI: 10.17116/patol20248604158

A literature review reflects data on the mechanisms of pulmonary fibrosis after a novel coronavirus infection associated with the SARS-COV2 virus. Factors contributing to post-COVID lung remodeling are considered. According to the literature, in the mechanism of pulmonary fibrosis, during the course of the disease and during the recovery period, both direct viral damage and death of alveolocytes and endothelium, the development of a systemic inflammatory reaction due to inadequate secretion of cytokines, especially type 2, which are activators of the proliferation of fibroblasts and myofibroblasts, are important. The influence of angiogenesis disorders and vascular dysfunction on pneumofibrosis was noted. Attention is also paid to the relationship between the development of pulmonary fibrosis and abnormal activation of the renin-angiotensin-aldosterone system. In combination with the action of many factors, especially germinal ones, an imbalance between profibrogenic and antifibrogenic action develops and fibrosis occurs.