Cellular Senescence in Lung Fibrosis
Fibrosing interstitial lung diseases (ILDs) are chronic and ultimately fatal age-related lung diseases characterized by the progressive and irreversible accumulation of scar tissue in the lung parenchyma. Over the past years, significant progress has been made in our incomplete understanding of the...
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| Format: | Article |
| Language: | English |
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MDPI AG
2021-06-01
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| Series: | International Journal of Molecular Sciences |
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| Online Access: | https://www.mdpi.com/1422-0067/22/13/7012 |
| _version_ | 1797528429726269440 |
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| author | Fernanda Hernandez-Gonzalez Rosa Faner Mauricio Rojas Alvar Agustí Manuel Serrano Jacobo Sellarés |
| author_facet | Fernanda Hernandez-Gonzalez Rosa Faner Mauricio Rojas Alvar Agustí Manuel Serrano Jacobo Sellarés |
| author_sort | Fernanda Hernandez-Gonzalez |
| collection | DOAJ |
| description | Fibrosing interstitial lung diseases (ILDs) are chronic and ultimately fatal age-related lung diseases characterized by the progressive and irreversible accumulation of scar tissue in the lung parenchyma. Over the past years, significant progress has been made in our incomplete understanding of the pathobiology underlying fibrosing ILDs, in particular in relation to diverse age-related processes and cell perturbations that seem to lead to maladaptation to stress and susceptibility to lung fibrosis. Growing evidence suggests that a specific biological phenomenon known as cellular senescence plays an important role in the initiation and progression of pulmonary fibrosis. Cellular senescence is defined as a cell fate decision caused by the accumulation of unrepairable cellular damage and is characterized by an abundant pro-inflammatory and pro-fibrotic secretome. The senescence response has been widely recognized as a beneficial physiological mechanism during development and in tumour suppression. However, recent evidence strengthens the idea that it also drives degenerative processes such as lung fibrosis, most likely by promoting molecular and cellular changes in chronic fibrosing processes. Here, we review how cellular senescence may contribute to lung fibrosis pathobiology, and we highlight current and emerging therapeutic approaches to treat fibrosing ILDs by targeting cellular senescence. |
| first_indexed | 2024-03-10T09:58:12Z |
| format | Article |
| id | doaj.art-e964a3aa51284b879b0c1b67eca89d91 |
| institution | Directory Open Access Journal |
| issn | 1661-6596 1422-0067 |
| language | English |
| last_indexed | 2024-03-10T09:58:12Z |
| publishDate | 2021-06-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | International Journal of Molecular Sciences |
| spelling | doaj.art-e964a3aa51284b879b0c1b67eca89d912023-11-22T02:12:52ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672021-06-012213701210.3390/ijms22137012Cellular Senescence in Lung FibrosisFernanda Hernandez-Gonzalez0Rosa Faner1Mauricio Rojas2Alvar Agustí3Manuel Serrano4Jacobo Sellarés5Department of Pulmonology, ICR, Hospital Clinic, 08036 Barcelona, SpainInstituto de Investigaciones Biomédicas August Pi i Sunyer (IDIBAPS), 08036 Barcelona, SpainDivision of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, The Ohio State University Wexner Medical Center, Columbus, OH 43210, USADepartment of Pulmonology, ICR, Hospital Clinic, 08036 Barcelona, SpainInstitute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology (BIST), 08028 Barcelona, SpainDepartment of Pulmonology, ICR, Hospital Clinic, 08036 Barcelona, SpainFibrosing interstitial lung diseases (ILDs) are chronic and ultimately fatal age-related lung diseases characterized by the progressive and irreversible accumulation of scar tissue in the lung parenchyma. Over the past years, significant progress has been made in our incomplete understanding of the pathobiology underlying fibrosing ILDs, in particular in relation to diverse age-related processes and cell perturbations that seem to lead to maladaptation to stress and susceptibility to lung fibrosis. Growing evidence suggests that a specific biological phenomenon known as cellular senescence plays an important role in the initiation and progression of pulmonary fibrosis. Cellular senescence is defined as a cell fate decision caused by the accumulation of unrepairable cellular damage and is characterized by an abundant pro-inflammatory and pro-fibrotic secretome. The senescence response has been widely recognized as a beneficial physiological mechanism during development and in tumour suppression. However, recent evidence strengthens the idea that it also drives degenerative processes such as lung fibrosis, most likely by promoting molecular and cellular changes in chronic fibrosing processes. Here, we review how cellular senescence may contribute to lung fibrosis pathobiology, and we highlight current and emerging therapeutic approaches to treat fibrosing ILDs by targeting cellular senescence.https://www.mdpi.com/1422-0067/22/13/7012pulmonary fibrosissenescencesenolyticssenomorphicsaging |
| spellingShingle | Fernanda Hernandez-Gonzalez Rosa Faner Mauricio Rojas Alvar Agustí Manuel Serrano Jacobo Sellarés Cellular Senescence in Lung Fibrosis International Journal of Molecular Sciences pulmonary fibrosis senescence senolytics senomorphics aging |
| title | Cellular Senescence in Lung Fibrosis |
| title_full | Cellular Senescence in Lung Fibrosis |
| title_fullStr | Cellular Senescence in Lung Fibrosis |
| title_full_unstemmed | Cellular Senescence in Lung Fibrosis |
| title_short | Cellular Senescence in Lung Fibrosis |
| title_sort | cellular senescence in lung fibrosis |
| topic | pulmonary fibrosis senescence senolytics senomorphics aging |
| url | https://www.mdpi.com/1422-0067/22/13/7012 |
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