Smoking accelerates aging of the small airway epithelium
Open accessAbstract
BACKGROUND: Aging involves multiple biologically complex processes characterized by a decline in cellular homeostasis over time leading to a loss and impairment of physiological integrity and function. Specific cellular hallmarks of aging include abnormal gene expression patterns, shortened telomeres and associated biological dysfunction. Like all organs, the lung demonstrates both physiological and structural changes with age that result in a progressive decrease in lung function in healthy individuals. Cigarette smoking accelerates lung function decline over time, suggesting smoking accelerates aging of the lung. Based on this data, we hypothesized that cigarette smoking accelerates the aging of the small airway epithelium, the cells that take the initial brunt of inhaled toxins from the cigarette smoke and one of the primary sites of pathology associated with cigarette smoking. METHODS: Using the sensitive molecular parameters of aging-related gene expression and telomere length, the aging process of the small airway epithelium was assessed in age matched healthy nonsmokers and healthy smokers with no physical manifestation of lung disease or abnormalities in lung function. RESULTS: Analysis of a 73 gene aging signature demonstrated that smoking significantly dysregulates 18 aging-related genes in the small airway epithelium. In an independent cohort of male subjects, smoking significantly reduced telomere length in the small airway epithelium of smokers by 14% compared to nonsmokers. CONCLUSION: These data provide biologic evidence that smoking accelerates aging of the small airway epithelium.
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
DNA damage from compounds such as cigarette smoke and telomere shortening due to increased demand for injured airway epithelium repair can result in disease-related senescence and generation of a secondary subset of senescent cells.
“DNA damage in response to compounds, such as those present in cigarette smoke, as well as telomere shortening due to increased demand for injured airway epithelium repair, can result in disease-related senescence and subsequent generation of a secondary subset of senescent cells (5).”
From Aging and Lung Disease (2020) · cites this paper as [5]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
The citation lists haven’t been fetched yet
References 65 · Cited by 87
- Authors
- Walters, M. S., De, B. P., Salit, J., Buro-Auriemma, L. J., Wilson, T., Rogalski, A. M., Lief, L., Hackett, N. R., Staudt, M. R., Tilley, A. E., Harvey, B.-G., Kaner, R. J., Mezey, J. G., Ashbridge, B., Moore, M. A. S., & Crystal, R. G.
- Affiliations
- Weill Cornell Medicine (US)
- Memorial Sloan Kettering Cancer Center (US)
- Corresponding author
- Crystal, Ronald G
- ORCID
- Venue
- Respiratory Research
- Published
- 2014-09-24
- Volume
- 15
- Issue
- 1
- Pages
- 94-94
- ISSN
- 1465-9921 (ISSN-L)
- 1465-993X
- PMC
- PMC4189169
- OpenAlex
- W2126263734
- Cited by
- 87
- References
- 65
- Citations by year
- 2026: 6 · 2025: 6 · 2024: 7 · 2023: 5 · 2022: 3 · 2021: 16 · 2020: 9 · 2019: 7 · 2018: 10 · 2017: 1 · 2016: 6 · 2015: 11
- FWCI
- 4.00
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Respiratory Research (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (UL1TR000457, TR000457, RR024143, HL084936)
- National Heart, Lung, and Blood Institute (K23HL103837, R01HL107882, P50HL084936, T32HL094284)
- National Cancer Institute (P30CA008748)
- National Center for Research Resources (UL1RR024143)
- National Center for Advancing Translational Sciences
- Topics
- Health Sciences › Medicine › Physiology › Smoking Behavior and Cessation
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Chronic Obstructive Pulmonary Disease (COPD) Research
- Keywords
- cigarette smoking, aging, small airway epithelium, telomere length, age-related gene expression, lung aging, gene expression signatures, lung function decline, cellular senescence
- MeSH terms
- Adult, Epithelial Cells, Female, Gene Expression Regulation, Humans, Male, Middle Aged, RNA, Messenger, Smoke, Smoking, Case-Control Studies, Telomere, Cellular Senescence, Respiratory Mucosa, Gene Expression Profiling, Telomere Shortening
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
