ArticlePloS one2013
Aging does not enhance experimental cigarette smoke-induced COPD in the mouse.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- Fueling the fire: metabolic dysfunction and senescence as drivers of lung aging and disease.Physiological reviews · 2026Review
- Short-Term and Long-Term Effects of Electronic Cigarettes on Mouse Lungs Following Nose-Only Exposures.Chemical research in toxicology · 2025Article
- Impact of electronic cigarette vaping on the cardiovascular function in young and old rats.Scientific reports · 2024Article
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- Review
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- Lung regeneration: implications of the diseased niche and ageing.European respiratory review : an official journal of the European Respiratory Society · 2020Review
- Sex differences in lymphoid follicles in COPD airways.Respiratory research · 2020Article
- Article
- Reduced expression of the Ion channel CFTR contributes to airspace enlargement as a consequence of aging and in response to cigarette smoke in mice.Respiratory research · 2019Article
- Club cell protein 16 (Cc16) deficiency increases inflamm-aging in the lungs of mice.Physiological reports · 2018Article
- Lung cellular senescence is independent of aging in a mouse model of COPD/emphysema.Scientific reports · 2018Article
- Honokiol protects skin cells against inflammation, collagenolysis, apoptosis, and senescence caused by cigarette smoke damage.International journal of dermatology · 2017Article
- Attenuating immune pathology using a microbial-based intervention in a mouse model of cigarette smoke-induced lung inflammation.Respiratory research · 2017Article
- Combined Effects of in Utero and Adolescent Tobacco Smoke Exposure on Lung Function in C57Bl/6J Mice.Environmental health perspectives · 2017Article
- Age and Small Airway Imaging Abnormalities in Subjects with and without Airflow Obstruction in SPIROMICS.American journal of respiratory and critical care medicine · 2017Article
- Experimental animal models for COPD: a methodological review.Tobacco induced diseases · 2017Review
- Article
- The Isosteroid Alkaloid Imperialine from Bulbs of Fritillaria cirrhosa Mitigates Pulmonary Functional and Structural Impairment and Suppresses Inflammatory Response in a COPD-Like Rat Model.Mediators of inflammation · 2016Article
- Soluble extracellular Klotho decreases sensitivity to cigarette smoke induced cell death in human lung epithelial cells.Toxicology in vitro : an international journal published in association with BIBRA · 2015Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
It has been proposed that the development of COPD is driven by premature aging/premature senescence of lung parenchyma cells. There are data suggesting that old mice develop a greater inflammatory and lower anti-oxidant response after cigarette smoke compared to young mice, but whether these differences actually translate into greater levels of disease is unknown. We exposed C57Bl/6 female mice to daily cigarette smoke for 6 months starting at age 3 months (Ayoung@) or age 12 months (Aold@), with air-exposed controls. There were no differences in measures of airspace size between the two control groups and cigarette smoke induced exactly the same amount of emphysema in young and old. The severity of smoke-induced small airway remodeling using various measures was identical in both groups. Smoke increased numbers of tissue macrophages and neutrophils and levels of 8-hydroxyguanosine, a marker of oxidant damage, but there were no differences between young and old. Gene expression studies using laser capture microdissected airways and parenchyma overall showed a trend to lower levels in older animals and a somewhat lesser response to cigarette smoke in both airways and parenchyma but the differences were usually not marked. Telomere length was greatest in young control mice and was decreased by both smoking and age. The senescence marker p21(Waf1) was equally upregulated by smoke in young and old, but p16(INK4a), another senescence marker, was not upregulated at all. We conclude, in this model, animal age does not affect the development of emphysema and small airway remodeling.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.