Senescence in Pulmonary Fibrosis: Between Aging and Exposure
To date, chronic pulmonary pathologies represent the third leading cause of death in the elderly population. Evidence-based projections suggest that >65 (years old) individuals will account for approximately a quarter of the world population before the turn of the century. Genomic instability...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2020-11-01
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| Series: | Frontiers in Medicine |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fmed.2020.606462/full |
| _version_ | 1818228361138274304 |
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| author | Alessandro Venosa |
| author_facet | Alessandro Venosa |
| author_sort | Alessandro Venosa |
| collection | DOAJ |
| description | To date, chronic pulmonary pathologies represent the third leading cause of death in the elderly population. Evidence-based projections suggest that >65 (years old) individuals will account for approximately a quarter of the world population before the turn of the century. Genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication, are described as the nine “hallmarks” that govern cellular fitness. Any deviation from the normal pattern initiates a complex cascade of events culminating to a disease state. This blueprint, originally employed to describe aberrant changes in cancer cells, can be also used to describe aging and fibrosis. Pulmonary fibrosis (PF) is the result of a progressive decline in injury resolution processes stemming from endogenous (physiological decline or somatic mutations) or exogenous stress. Environmental, dietary or occupational exposure accelerates the pathogenesis of a senescent phenotype based on (1) window of exposure; (2) dose, duration, recurrence; and (3) cells type being targeted. As the lung ages, the threshold to generate an irreversibly senescent phenotype is lowered. However, we do not have sufficient knowledge to make accurate predictions. In this review, we provide an assessment of the literature that interrogates lung epithelial, mesenchymal, and immune senescence at the intersection of aging, environmental exposure and pulmonary fibrosis. |
| first_indexed | 2024-12-12T10:01:29Z |
| format | Article |
| id | doaj.art-8178999620af420a8e22435e4b144fc2 |
| institution | Directory Open Access Journal |
| issn | 2296-858X |
| language | English |
| last_indexed | 2024-12-12T10:01:29Z |
| publishDate | 2020-11-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Medicine |
| spelling | doaj.art-8178999620af420a8e22435e4b144fc22022-12-22T00:27:59ZengFrontiers Media S.A.Frontiers in Medicine2296-858X2020-11-01710.3389/fmed.2020.606462606462Senescence in Pulmonary Fibrosis: Between Aging and ExposureAlessandro VenosaTo date, chronic pulmonary pathologies represent the third leading cause of death in the elderly population. Evidence-based projections suggest that >65 (years old) individuals will account for approximately a quarter of the world population before the turn of the century. Genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication, are described as the nine “hallmarks” that govern cellular fitness. Any deviation from the normal pattern initiates a complex cascade of events culminating to a disease state. This blueprint, originally employed to describe aberrant changes in cancer cells, can be also used to describe aging and fibrosis. Pulmonary fibrosis (PF) is the result of a progressive decline in injury resolution processes stemming from endogenous (physiological decline or somatic mutations) or exogenous stress. Environmental, dietary or occupational exposure accelerates the pathogenesis of a senescent phenotype based on (1) window of exposure; (2) dose, duration, recurrence; and (3) cells type being targeted. As the lung ages, the threshold to generate an irreversibly senescent phenotype is lowered. However, we do not have sufficient knowledge to make accurate predictions. In this review, we provide an assessment of the literature that interrogates lung epithelial, mesenchymal, and immune senescence at the intersection of aging, environmental exposure and pulmonary fibrosis.https://www.frontiersin.org/articles/10.3389/fmed.2020.606462/fullsenescencelung fibrosisepithelial cellsinflamm-agingimmune-senescenceaging |
| spellingShingle | Alessandro Venosa Senescence in Pulmonary Fibrosis: Between Aging and Exposure Frontiers in Medicine senescence lung fibrosis epithelial cells inflamm-aging immune-senescence aging |
| title | Senescence in Pulmonary Fibrosis: Between Aging and Exposure |
| title_full | Senescence in Pulmonary Fibrosis: Between Aging and Exposure |
| title_fullStr | Senescence in Pulmonary Fibrosis: Between Aging and Exposure |
| title_full_unstemmed | Senescence in Pulmonary Fibrosis: Between Aging and Exposure |
| title_short | Senescence in Pulmonary Fibrosis: Between Aging and Exposure |
| title_sort | senescence in pulmonary fibrosis between aging and exposure |
| topic | senescence lung fibrosis epithelial cells inflamm-aging immune-senescence aging |
| url | https://www.frontiersin.org/articles/10.3389/fmed.2020.606462/full |
| work_keys_str_mv | AT alessandrovenosa senescenceinpulmonaryfibrosisbetweenagingandexposure |