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Updated: Jun 18, 2025
06:03
Oropharyngeal Administration of Bleomycin in the Murine Model of Pulmonary Fibrosis
Published on: May 9, 2025
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[Pathogenesis of pulmonary fibrosis].
1Academician I.P. Pavlov First St. Petersburg State Medical University, St. Petersburg, Russia.
Arkhiv Patologii
|July 29, 2024
Summary
This review explores how SARS-CoV-2 infection causes pulmonary fibrosis. Key factors include direct lung damage, inflammation, and renin-angiotensin system imbalance, leading to lung remodeling.
Area of Science:
- Pulmonology
- Virology
- Pathology
Background:
- Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection can lead to long-term lung damage.
- Pulmonary fibrosis, a condition of lung scarring, is a significant concern following COVID-19.
Purpose of the Study:
- To review the mechanisms driving pulmonary fibrosis post-SARS-CoV-2 infection.
- To identify key factors contributing to lung remodeling after COVID-19.
Main Methods:
- Literature review of existing studies on SARS-CoV-2 and pulmonary fibrosis.
- Analysis of data on viral, inflammatory, vascular, and hormonal pathways involved.
Main Results:
- Direct viral damage to lung cells (alveolocytes and endothelium) contributes to fibrosis.
- Systemic inflammation, particularly involving type 2 cytokines, promotes fibroblast proliferation.
- Disrupted angiogenesis, vascular dysfunction, and abnormal renin-angiotensin-aldosterone system activity are implicated.
Conclusions:
- Pulmonary fibrosis post-COVID-19 results from a complex interplay of direct injury, inflammation, and hormonal dysregulation.
- Understanding these mechanisms is crucial for developing targeted therapies for post-COVID lung remodeling.
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