AI Article Synopsis

  • The literature review discusses how COVID-19 can lead to pulmonary fibrosis by exploring the underlying mechanisms associated with the SARS-COV2 virus infection.
  • Key factors contributing to lung remodeling after COVID-19 include direct damage from the virus, inflammatory responses due to cytokine imbalance, and issues with blood vessel function.
  • The review highlights that the abnormal activation of the renin-angiotensin-aldosterone system, combined with other contributing factors, creates an imbalance that promotes fibrosis in the lungs.

Article Abstract

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.

Download full-text PDF

Source
http://dx.doi.org/10.17116/patol20248604158DOI Listing

Publication Analysis

Top Keywords

pulmonary fibrosis
12
[pathogenesis pulmonary
4
pulmonary fibrosis]
4
fibrosis] literature
4
literature review
4
review reflects
4
reflects data
4
data mechanisms
4
mechanisms pulmonary
4
fibrosis
4

Similar Publications

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!