Cellular and Molecular Mechanism of Pulmonary Fibrosis Post-COVID-19: Focus on Galectin-1, -3, -8, -9
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-C...
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MDPI AG
2022-07-01
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| Series: | International Journal of Molecular Sciences |
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| Online Access: | https://www.mdpi.com/1422-0067/23/15/8210 |
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| author | Daniela Oatis Erika Simon-Repolski Cornel Balta Alin Mihu Gorizio Pieretti Roberto Alfano Luisa Peluso Maria Consiglia Trotta Michele D’Amico Anca Hermenean |
| author_facet | Daniela Oatis Erika Simon-Repolski Cornel Balta Alin Mihu Gorizio Pieretti Roberto Alfano Luisa Peluso Maria Consiglia Trotta Michele D’Amico Anca Hermenean |
| author_sort | Daniela Oatis |
| collection | DOAJ |
| description | 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. |
| first_indexed | 2024-03-09T12:36:02Z |
| format | Article |
| id | doaj.art-78f696f2df704052b688d53fd7a29014 |
| institution | Directory Open Access Journal |
| issn | 1661-6596 1422-0067 |
| language | English |
| last_indexed | 2024-03-09T12:36:02Z |
| publishDate | 2022-07-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | International Journal of Molecular Sciences |
| spelling | doaj.art-78f696f2df704052b688d53fd7a290142023-11-30T22:24:32ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672022-07-012315821010.3390/ijms23158210Cellular and Molecular Mechanism of Pulmonary Fibrosis Post-COVID-19: Focus on Galectin-1, -3, -8, -9Daniela Oatis0Erika Simon-Repolski1Cornel Balta2Alin Mihu3Gorizio Pieretti4Roberto Alfano5Luisa Peluso6Maria Consiglia Trotta7Michele D’Amico8Anca Hermenean9Department of Infectious Disease, Faculty of Medicine, Vasile Goldis Western University of Arad, 310414 Arad, RomaniaDoctoral School of Medicine, Vasile Goldis Western University of Arad, 310414 Arad, Romania“Aurel Ardelean” Institute of Life Sciences, Vasile Goldis Western University of Arad, 310144 Arad, RomaniaDepartment of Microbiology, Faculty of Medicine, Vasile Goldis Western University of Arad, 310414 Arad, RomaniaDepartment of Plastic Surgery, University of Campania “Luigi Vanvitelli”, 80138 Naples, ItalyDepartment of Advanced Medical and Surgical Sciences “DAMSS”, University of Campania “Luigi Vanvitelli”, 80138 Naples, ItalyDepartment of Experimental Medicine, University of Campania “Luigi Vanvitelli”, 80138 Naples, ItalyDepartment of Experimental Medicine, University of Campania “Luigi Vanvitelli”, 80138 Naples, ItalyDepartment of Experimental Medicine, University of Campania “Luigi Vanvitelli”, 80138 Naples, Italy“Aurel Ardelean” Institute of Life Sciences, Vasile Goldis Western University of Arad, 310144 Arad, RomaniaPulmonary 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.https://www.mdpi.com/1422-0067/23/15/8210COVID-19pulmonary fibrosisgalectinmyofibroblasts |
| spellingShingle | Daniela Oatis Erika Simon-Repolski Cornel Balta Alin Mihu Gorizio Pieretti Roberto Alfano Luisa Peluso Maria Consiglia Trotta Michele D’Amico Anca Hermenean Cellular and Molecular Mechanism of Pulmonary Fibrosis Post-COVID-19: Focus on Galectin-1, -3, -8, -9 International Journal of Molecular Sciences COVID-19 pulmonary fibrosis galectin myofibroblasts |
| title | Cellular and Molecular Mechanism of Pulmonary Fibrosis Post-COVID-19: Focus on Galectin-1, -3, -8, -9 |
| title_full | Cellular and Molecular Mechanism of Pulmonary Fibrosis Post-COVID-19: Focus on Galectin-1, -3, -8, -9 |
| title_fullStr | Cellular and Molecular Mechanism of Pulmonary Fibrosis Post-COVID-19: Focus on Galectin-1, -3, -8, -9 |
| title_full_unstemmed | Cellular and Molecular Mechanism of Pulmonary Fibrosis Post-COVID-19: Focus on Galectin-1, -3, -8, -9 |
| title_short | Cellular and Molecular Mechanism of Pulmonary Fibrosis Post-COVID-19: Focus on Galectin-1, -3, -8, -9 |
| title_sort | cellular and molecular mechanism of pulmonary fibrosis post covid 19 focus on galectin 1 3 8 9 |
| topic | COVID-19 pulmonary fibrosis galectin myofibroblasts |
| url | https://www.mdpi.com/1422-0067/23/15/8210 |
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