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Review
. 2022 Jul 26;23(15):8210.
doi: 10.3390/ijms23158210.

Cellular and Molecular Mechanism of Pulmonary Fibrosis Post-COVID-19: Focus on Galectin-1, -3, -8, -9

Daniela Oatis  1   2 , Erika Simon-Repolski  3   4 , Cornel Balta  5 , Alin Mihu  6 , Gorizio Pieretti  7 , Roberto Alfano  8 , Luisa Peluso  9 , Maria Consiglia Trotta  9 , Michele D'Amico  9 , Anca Hermenean  5   10
Affiliations
Review

Cellular and Molecular Mechanism of Pulmonary Fibrosis Post-COVID-19: Focus on Galectin-1, -3, -8, -9

Daniela Oatis et al. Int J Mol Sci. .

Abstract

Pulmonary fibrosis is a consequence of the pathological accumulation of extracellular matrix (ECM), which finally leads to lung scarring. Although the pulmonary fibrogenesis is almost known, the last two years of the COVID-19 pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and its post effects added new particularities which need to be explored. Many questions remain about how pulmonary fibrotic changes occur within the lungs of COVID-19 patients, and whether the changes will persist long term or are capable of resolving. This review brings together existing knowledge on both COVID-19 and pulmonary fibrosis, starting with the main key players in promoting pulmonary fibrosis, such as alveolar and endothelial cells, fibroblasts, lipofibroblasts, and macrophages. Further, we provide an overview of the main molecular mechanisms driving the fibrotic process in connection with Galactin-1, -3, -8, and -9, together with the currently approved and newly proposed clinical therapeutic solutions given for the treatment of fibrosis, based on their inhibition. The work underlines the particular pathways and processes that may be implicated in pulmonary fibrosis pathogenesis post-SARS-CoV-2 viral infection. The recent data suggest that galectin-1, -3, -8, and -9 could become valuable biomarkers for the diagnosis and prognosis of lung fibrosis post-COVID-19 and promising molecular targets for the development of new and original therapeutic tools to treat the disease.

Keywords: COVID-19; galectin; myofibroblasts; pulmonary fibrosis.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Schematic representation of the galectin-1, -3, -8, and -9 role in the mechanism regulating myofibroblasts activation in pulmonary fibrosis post-COVID-19. macrophages (MG); type I alveolar epithelial cells (AT1); type II alveolar epithelial cells (AT2); dendritic cell (DC); epithelial-mesenchymal transition (EMT); endothelial-mesenchymal transition (EndMT); myofibroblast (Mfb); fibroblast (Fb); lipofibroblasts (Lfb); monocyte (Mo); platelet (Pt); activated platelet (aPt); polymorphonuclear neutrophil (PMN); neutrophil extracellular trap (NETs); angiotensin-converting enzyme 2 receptor (ACE2); mesenchymal stromal cells (MSCs); platelet-derived growth factor (PDGF); transforming growth factor beta1 (TGF-β). This figure was created with BioRender.com (accessed on 18 July 2022).
See this image and copyright information in PMC

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This research received no external funding.