Pirfenidone and post-Covid-19 pulmonary fibrosis: invoked again for realistic goals
UNIVERSAL IDENTIFIER: http://hdl.handle.net/11093/4600
EDITED VERSION: https://link.springer.com/10.1007/s10787-022-01027-6
DOCUMENT TYPE: article
Pirfenidone (PFN) is an anti-fbrotic drug with signifcant anti-infammatory property used for treatment of fbrotic conditions such as idiopathic pulmonary fbrosis (IPF). In the coronavirus disease 2019 (Covid-19) era, severe acute respiratory syndrome 2 (SARS-CoV-2) could initially lead to acute lung injury (ALI) and in severe cases may cause acute respiratory distress syndrome (ARDS) which is usually resolved with normal lung function. However, some cases of ALI and ARDS are progressed to the more severe critical stage of pulmonary fbrosis commonly named post-Covid-19 pulmonary fbrosis which needs an urgent address and proper management. Therefore, the objective of the present study was to highlight the potential role of PFN in the management of post-Covid-19 pulmonary fbrosis. The precise mechanism of post-Covid-19 pulmonary fbrosis is related to the activation of transforming growth factor beta (TGF-β1), which activates the release of extracellular proteins, fbroblast proliferation, fbroblast migration and myofbroblast conversion. PFN inhibits accumulation and recruitment of infammatory cells, fbroblast proliferation, deposition of extracellular matrix in response to TGFβ1 and other pro-infammatory cytokines. In addition, PFN suppresses furin (TGFβ1 convertase activator) a protein efector involved in the entry of SARS-CoV-2 and activation of TGFβ1, and thus PFN reduces the pathogenesis of SARS-CoV-2. Besides, PFN modulates signaling pathways such as Wingless/Int (Wnt/β-catenin), Yes-Associated Protein (YAP)/Transcription CoActivator PDZ Binding Motif (TAZ) and Hippo Signaling Pathways that are involved in the pathogenesis of post-Covid-19 pulmonary fbrosis. In conclusion, the anti-infammatory and anti-fbrotic properties of PFN may attenuate post-Covid-19 pulmonary fbrosis.
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