Rybakova M G, Myurzep A E
Academician I.P. Pavlov First St. Petersburg State Medical University, St. Petersburg, Russia.
Arkh Patol. 2024;86(4):58-63. 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.
一篇文献综述反映了与严重急性呼吸综合征冠状病毒2（SARS-CoV-2）病毒相关的新型冠状病毒感染后肺纤维化机制的数据。文中考虑了导致新冠后肺重塑的因素。根据文献，在肺纤维化机制中，在疾病过程和恢复期，肺泡细胞和内皮细胞的直接病毒损伤和死亡、由于细胞因子分泌不足，尤其是2型细胞因子（成纤维细胞和平滑肌成纤维细胞增殖的激活剂）导致的全身炎症反应的发展都很重要。文中指出了血管生成障碍和血管功能障碍对肺纤维化的影响。还关注了肺纤维化的发展与肾素-血管紧张素-醛固酮系统异常激活之间的关系。多种因素，尤其是起始因素共同作用，导致促纤维化和抗纤维化作用失衡，进而发生纤维化。
