Perspectives on Post-COVID-19 Pulmonary Fibrosis Treatment

Abstract

Pulmonary fibrosis, a critical outcome of chronic inflammatory diseases, has gained prominence in the context of post-coronavirus (post-COVID-19) complications. This review delves into the multifaceted landscape of post-COVID-19 pulmonary fibrosis, elucidating the intricate molecular mechanisms underlying its pathogenesis and highlighting promising therapeutic avenues. Examining the aftermath of severe acute respiratory syndrome-2 (SARS-CoV-2) infection, the review reveals key signaling pathways implicated in the fibrotic cascade. Drawing parallels with previous coronavirus outbreaks enhances our understanding of the distinctive features of post-COVID-19 fibrosis. Antifibrotic drugs, like pirfenidone and nintedanib, take center stage; their mechanisms of action and potential applications in post-COVID-19 cases are thoroughly explored. Beyond the established treatments, this review investigates emerging therapeutic modalities, including anti-interleukin agents, immunosuppressants, and experimental compounds, like buloxybutide, saracatinib, sirolimus, and resveratrol. Emphasizing the critical importance of early intervention, this review highlights the dynamic nature of post-COVID-19 pulmonary fibrosis research. In conclusion, the synthesis of current knowledge offers a foundation for advancing our approaches to the prevention and treatment of these consequential sequelae of COVID-19.

Keywords: antifibrotic; fibrosis; nintedanib; pirfenidone; post-COVID-19; pulmonary; treatment.

Figure 2

The mechanisms of action of pirfenidone.

Figure 1

Signal pathways linked to post-COVID-19 pulmonary fibrosis pathophysiology. Legend: YAP—yes-associated protein 1; TAZ—transcriptional coactivator with PDZ-binding motif; TLR—toll-like receptor; TGF-β—transforming growth factor-beta; MAPK—mitogen-activated protein kinase; WNT—wingless/Int; PDGF—platelet-derived growth factor; VEGF—vascular endothelial growth factor; NF-κB—nuclear factor-kappa B; ET-1—endothelin-1; HIF—hypoxia-inducible factor.