DOI: 10.3390/biomedicines12030639 ISSN: 2227-9059

The Role of Cytokines and Molecular Pathways in Lung Fibrosis following SARS-CoV-2 Infection: A Physiopathologic (Re)view

Mihai Lazar, Mihai Sandulescu, Ecaterina Constanta Barbu, Cristina Emilia Chitu-Tisu, Darie Ioan Andreescu, Andreea Nicoleta Anton, Teodora Maria Erculescu, Alexandru Mihai Petre, George Theodor Duca, Vladimir Simion, Isabela Felicia Padiu, Cosmina Georgiana Pacurar, Ruxandra Rosca, Teodor Mihai Simian, Constantin Adrian Oprea, Daniela Adriana Ion
  • General Biochemistry, Genetics and Molecular Biology
  • Medicine (miscellaneous)

SARS-CoV-2 infection is a significant health concern that needs to be addressed not only during the initial phase of infection but also after hospitalization. This is the consequence of the various pathologies associated with long COVID-19, which are still being studied and researched. Lung fibrosis is an important complication after COVID-19, found in up to 71% of patients after discharge. Our research is based on scientific articles indexed in PubMed; in the selection process, we used the following keywords: “lung fibrosis”, “fibrosis mediators”, “fibrosis predictors”, “COVID-19”, “SARS-CoV-2 infection”, and “long COVID-19”. In this narrative review, we aimed to discuss the current understanding of the mechanisms of initiation and progression of post-COVID-19 lung fibrosis (PC-19-LF) and the risk factors for its occurrence. The pathogenesis of pulmonary fibrosis involves various mediators such as TGF-β, legumain, osteopontin, IL-4, IL-6, IL-13, IL-17, TNF-α, Gal-1, Gal-3, PDGF, and FGFR-1. The key cellular effectors involved in COVID-19 lung fibrosis are macrophages, epithelial alveolar cells, neutrophils, and fibroblasts. The main fibrosis pathways in SARS-CoV-2 infection include hypoxemia-induced fibrosis, macrophage-induced fibrosis, and viral-fibroblast interaction-induced fibrosis.

More from our Archive