COVID-19 Infection May Drive EC-like Myofibroblasts towards Myofibroblasts to Contribute to Pulmonary Fibrosis

Int J Mol Sci. 2023 Jul 15;24(14):11500. doi: 10.3390/ijms241411500.

Abstract

COVID-19 has an extensive impact on Homo sapiens globally. Patients with COVID-19 are at an increased risk of developing pulmonary fibrosis. A previous study identified that myofibroblasts could be derived from pulmonary endothelial lineage cells as an important cell source that contributes to pulmonary fibrosis. Here, we analyzed publicly available data and showed that COVID-19 infection drove endothelial lineage cells towards myofibroblasts in pulmonary fibrosis of patients with COVID-19. We also discovered a similar differentiation trajectory in mouse lungs after viral infection. The results suggest that COVID-19 infection leads to the development of pulmonary fibrosis partly through the activation of endothelial cell (EC)-like myofibroblasts.

Keywords: COVID-19; endothelial cells; pulmonary fibrosis.

MeSH terms

  • Animals
  • COVID-19* / pathology
  • Cell Differentiation
  • Endothelial Cells / pathology
  • Fibrosis
  • Lung
  • Mice
  • Myofibroblasts / pathology
  • Pulmonary Fibrosis* / etiology
  • Pulmonary Fibrosis* / pathology