ArticleScientific reports2018
Lung cellular senescence is independent of aging in a mouse model of COPD/emphysema.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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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.
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Who cites it
43 citing papers in PubMed, 59 citations in OpenAlex.
- A critical role for mitochondrial dynamics in cigarette smoke condensate-induced RPE senescence.Free radical biology & medicine · 2026Article
- Fueling the fire: metabolic dysfunction and senescence as drivers of lung aging and disease.Physiological reviews · 2026Review
- Heterogeneity of Cellular Senescence, Senotyping, and Targeting by Senolytics and Senomorphics in Lung Diseases.International journal of molecular sciences · 2025Review
- Cadmium exposure triggers vimentin phosphorylation via SIRT6-regulated AKT/PI3K signaling pathway in COPD.European journal of cell biology · 2025Article
- Cellular senescence in adult pulmonary hypertension: current state and future challenges.European respiratory review : an official journal of the European Respiratory Society · 2025Review
- Sex Differences in Chronic Obstructive Pulmonary Disease: Implications for Pathogenesis, Diagnosis, and Treatment.International journal of molecular sciences · 2025Review
- Diagnostic Challenges and Pathogenetic Differences in Biomass-Smoke-Induced versus Tobacco-Smoke-Induced COPD: A Comparative Review.Diagnostics (Basel, Switzerland) · 2024Review
- Article
- Club cell-specific telomere protection protein 1 (TPP1) protects against tobacco smoke-induced lung inflammation, xenobiotic metabolic dysregulation, and injurious responses.FASEB bioAdvances · 2024Article
- Alveolar type II epithelial cell FASN maintains lipid homeostasis in experimental COPD.JCI insight · 2023Article
- Characterization of a spontaneous mouse model of mild, accelerated aging via ECM degradation in emphysematous lungs.Scientific reports · 2023Article
- Clearance of senescent cells reverts the cigarette smoke-induced lung senescence and airspace enlargement in p16-3MR mice.Aging cell · 2023Article
- Age-related changes in lung function in National Center for Geriatrics and Gerontology Aging Farm C57BL/6N mice.Experimental animals · 2023Article
- Impact of aging on immune function in the pathogenesis of pulmonary diseases: potential for therapeutic targets.Expert review of respiratory medicine · 2023Review
- Oxidative Stress and Inflammation in Acute and Chronic Lung Injuries.Antioxidants (Basel, Switzerland) · 2023Review
- TLR9 Mediates Periodontal Aging by Fostering Senescence and Inflammaging.Journal of dental research · 2022Article
- Advanced age is associated with changes in alveolar macrophages and their responses to the stress of traumatic injury.Journal of leukocyte biology · 2022Article
- P16INK4A-More Than a Senescence Marker.Life (Basel, Switzerland) · 2022Review
- Senescence: Pathogenic Driver in Chronic Obstructive Pulmonary Disease.Medicina (Kaunas, Lithuania) · 2022Review
- Cellular Senescence in Aging Lungs and Diseases.Cells · 2022Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Cigarette smoke (CS) induces lung cellular senescence that plays an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD). How aging influences cellular senescence and other molecular hallmarks, and increases the risk of CS-induced damage remains unknown. We hypothesized that aging-associated changes in lungs worsen the COPD/emphysema by CS exposure. Younger and older groups of C57BL/6J mice were exposed to chronic CS for 6 months with respective age-matched air-exposed controls. CS caused a decline in lung function and affected the lung structure of both groups of mice. No alterations were observed in the induction of inflammatory mediators between the air-exposed younger and older controls, but aging increased the severity of CS-induced lung inflammation. Aging per se increased lung cellular senescence and significant changes in damage-associated molecular patterns marker S100A8. Gene transcript analysis using the nanoString nCounter showed a significant upregulation of key pro-senescence targets by CS (Mmp12, Ccl2, Cdkn2a, Tert, Wrn, and Bub1b). Aging independently influenced lung function and structure, as well as increased susceptibility to CS-induced inflammation in emphysema, but had a negligible effect on cellular senescence. Thus, aging solely does not contribute to the induction of cellular senescence by CS in a mouse model of COPD/emphysema.
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Registered trials
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