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Pirfenidone and post-Covid-19 pulmonary fibrosis: invoked again for realistic goals
Pirfenidone (PFN) is an anti-fibrotic drug with significant anti-inflammatory property used for treatment of fibrotic conditions such as idiopathic pulmonary fibrosis (IPF). In the coronavirus disease 2019 (Covid-19) era, severe acute respiratory syndrome 2 (SARS-CoV-2) could initially lead to acute...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Springer International Publishing
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9430017/ https://www.ncbi.nlm.nih.gov/pubmed/36044102 http://dx.doi.org/10.1007/s10787-022-01027-6 |
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author | Al-kuraishy, Hayder M. Batiha, Gaber El-Saber Faidah, Hani Al-Gareeb, Ali I. Saad, Hebatallah M. Simal-Gandara, Jesus |
author_facet | Al-kuraishy, Hayder M. Batiha, Gaber El-Saber Faidah, Hani Al-Gareeb, Ali I. Saad, Hebatallah M. Simal-Gandara, Jesus |
author_sort | Al-kuraishy, Hayder M. |
collection | PubMed |
description | Pirfenidone (PFN) is an anti-fibrotic drug with significant anti-inflammatory property used for treatment of fibrotic conditions such as idiopathic pulmonary fibrosis (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 fibrosis commonly named post-Covid-19 pulmonary fibrosis 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 fibrosis. The precise mechanism of post-Covid-19 pulmonary fibrosis is related to the activation of transforming growth factor beta (TGF-β1), which activates the release of extracellular proteins, fibroblast proliferation, fibroblast migration and myofibroblast conversion. PFN inhibits accumulation and recruitment of inflammatory cells, fibroblast proliferation, deposition of extracellular matrix in response to TGFβ1 and other pro-inflammatory cytokines. In addition, PFN suppresses furin (TGFβ1 convertase activator) a protein effector 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 Co-Activator PDZ Binding Motif (TAZ) and Hippo Signaling Pathways that are involved in the pathogenesis of post-Covid-19 pulmonary fibrosis. In conclusion, the anti-inflammatory and anti-fibrotic properties of PFN may attenuate post-Covid-19 pulmonary fibrosis. |
format | Online Article Text |
id | pubmed-9430017 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Springer International Publishing |
record_format | MEDLINE/PubMed |
spelling | pubmed-94300172022-09-01 Pirfenidone and post-Covid-19 pulmonary fibrosis: invoked again for realistic goals Al-kuraishy, Hayder M. Batiha, Gaber El-Saber Faidah, Hani Al-Gareeb, Ali I. Saad, Hebatallah M. Simal-Gandara, Jesus Inflammopharmacology Review Pirfenidone (PFN) is an anti-fibrotic drug with significant anti-inflammatory property used for treatment of fibrotic conditions such as idiopathic pulmonary fibrosis (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 fibrosis commonly named post-Covid-19 pulmonary fibrosis 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 fibrosis. The precise mechanism of post-Covid-19 pulmonary fibrosis is related to the activation of transforming growth factor beta (TGF-β1), which activates the release of extracellular proteins, fibroblast proliferation, fibroblast migration and myofibroblast conversion. PFN inhibits accumulation and recruitment of inflammatory cells, fibroblast proliferation, deposition of extracellular matrix in response to TGFβ1 and other pro-inflammatory cytokines. In addition, PFN suppresses furin (TGFβ1 convertase activator) a protein effector 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 Co-Activator PDZ Binding Motif (TAZ) and Hippo Signaling Pathways that are involved in the pathogenesis of post-Covid-19 pulmonary fibrosis. In conclusion, the anti-inflammatory and anti-fibrotic properties of PFN may attenuate post-Covid-19 pulmonary fibrosis. Springer International Publishing 2022-08-31 2022 /pmc/articles/PMC9430017/ /pubmed/36044102 http://dx.doi.org/10.1007/s10787-022-01027-6 Text en © The Author(s), under exclusive licence to Springer Nature Switzerland AG 2022, Springer Nature or its licensor holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic. |
spellingShingle | Review Al-kuraishy, Hayder M. Batiha, Gaber El-Saber Faidah, Hani Al-Gareeb, Ali I. Saad, Hebatallah M. Simal-Gandara, Jesus Pirfenidone and post-Covid-19 pulmonary fibrosis: invoked again for realistic goals |
title | Pirfenidone and post-Covid-19 pulmonary fibrosis: invoked again for realistic goals |
title_full | Pirfenidone and post-Covid-19 pulmonary fibrosis: invoked again for realistic goals |
title_fullStr | Pirfenidone and post-Covid-19 pulmonary fibrosis: invoked again for realistic goals |
title_full_unstemmed | Pirfenidone and post-Covid-19 pulmonary fibrosis: invoked again for realistic goals |
title_short | Pirfenidone and post-Covid-19 pulmonary fibrosis: invoked again for realistic goals |
title_sort | pirfenidone and post-covid-19 pulmonary fibrosis: invoked again for realistic goals |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9430017/ https://www.ncbi.nlm.nih.gov/pubmed/36044102 http://dx.doi.org/10.1007/s10787-022-01027-6 |
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