ArticleBMC genomics2019
RNA sequencing identifies common pathways between cigarette smoke exposure and replicative senescence in human airway epithelia.
Article in BMC genomics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 11 citations in OpenAlex.
- The Punicalagin Compound Mitigates Bronchial Epithelial Cell Senescence Induced by Cigarette Smoke Extract through the PAR2/mTOR Pathway.Current medicinal chemistry · 2025Article
- Multidimensional assessment of the biological effects of electronic cigarettes on lung bronchial epithelial cells.Scientific reports · 2024Article
- Airway Epithelium Senescence as a Driving Mechanism in COPD Pathogenesis.Biomedicines · 2023Review
- Computational screen to identify potential targets for immunotherapeutic identification and removal of senescence cells.Aging cell · 2023Article
- Recent evidence from omic analysis for redox signalling and mitochondrial oxidative stress in COPD.Journal of inflammation (London, England) · 2022Review
- Senescence: Pathogenic Driver in Chronic Obstructive Pulmonary Disease.Medicina (Kaunas, Lithuania) · 2022Review
- Systems approaches to investigate the role of NF-κB signaling in aging.The Biochemical journal · 2022Review
- Signaling pathway perturbation analysis for assessment of biological impact of cigarette smoke on lung cells.Scientific reports · 2021Article
Corrections and comments
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Authors and funding
13 authors at 6 institutions in 1 country.
Funding
Abstract
backgroundAging is affected by genetic and environmental factors, and cigarette smoking is strongly associated with accumulation of senescent cells. In this study, we wanted to identify genes that may potentially be beneficial for cell survival in response to cigarette smoke and thereby may contribute to development of cellular senescence.
resultsPrimary human bronchial epithelial cells from five healthy donors were cultured, treated with or without 1.5% cigarette smoke extract (CSE) for 24 h or were passaged into replicative senescence. Transcriptome changes were monitored using RNA-seq in CSE and non-CSE exposed cells and those passaged into replicative senescence. We found that, among 1534 genes differentially regulated during senescence and 599 after CSE exposure, 243 were altered in both conditions, representing strong enrichment. Pathways and gene sets overrepresented in both conditions belonged to cellular processes that regulate reactive oxygen species, proteasome degradation, and NF-κB signaling.
conclusionsOur results offer insights into gene expression responses during cellular aging and cigarette smoke exposure, and identify potential molecular pathways that are altered by cigarette smoke and may also promote airway epithelial cell senescence.
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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 Socratic graph.