2020
DOI: 10.1186/s12864-020-6712-z
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Abstract: Background: Lung aging is characterized by a number of structural alterations including fibrosis, chronic inflammation and the alteration of inflammatory cell composition. Chronic exposure to cigarette smoke (CS) is known to induce similar alterations and may contribute to premature lung aging. Additionally, aging and CS exposure are associated with transcriptional alterations in the lung. The current work aims to explore the interaction between age-and CS-associated transcriptomic perturbations and develop a … Show more

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Cited by 18 publications
(8 citation statements)
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“…Many of the components in tobacco smoke chemically react with oxygen to generate free radicals and inhibit protective antioxidants [20]. Through the combustion of noxious chemicals and generation of harmful reactive oxygen species (ROS), tobacco smoke induces widespread tissue damage in a manner that mimics biological aging (Table 1) [21].…”
Section: Tobacco Smokementioning
confidence: 99%
“…Many of the components in tobacco smoke chemically react with oxygen to generate free radicals and inhibit protective antioxidants [20]. Through the combustion of noxious chemicals and generation of harmful reactive oxygen species (ROS), tobacco smoke induces widespread tissue damage in a manner that mimics biological aging (Table 1) [21].…”
Section: Tobacco Smokementioning
confidence: 99%
“…Genotoxic stress causes premature hair greying . Smoking causes not only cancer but also premature aging in exposed organs (Choukrallah et al, 2020;. Radiation and mutagenic chemotherapy leads not only to therapy-related secondary cancer , but also to premature frailty, multi-morbidity and increased mortality , which has been attributed to the system-wide persistent accumulation of senescent cells .…”
Section: The Tumor Suppression Theory Of Aging 21 Overviewmentioning
confidence: 99%
“…There is extensive evidence that, although often well-tolerated, repeated toxic exposure promotes progressive genetic instability, epigenetic remodeling (i.e., cadmium); proteostatic and mitochondrial dysfunction (i.e., ozone); genesis of SASP (i.e., multi-walled nanotubes, asbestos); or all of the above (i.e., cigarette smoke and radiation) (82)(83)(84)(85)(86)(87). The (often) cyclical nature of environmental/occupational exposure is also linked to exhaustion of the stem cell reservoir, their depletion, and SASP (88)(89)(90).…”
Section: Dose Duration and Recurrence Of Exposurementioning
confidence: 99%
“…identify a signature spanning across age-and chemical-induced senescence. This machine learning approach using training datasets from chronic exposure to cigarette smoke and radiation, allowed to build a transcriptomic age model that accurately predicts chronological age in untreated mice and the deviations associated with certain exposures based on a 57-gene signature including Cyp1a1, Lcn2, MMPs, and immunoglobulins (87). There is no panacea or elixir to counter the effects of ageor chemical-induced senescence.…”
Section: Biological Signatures and Therapymentioning
confidence: 99%