ArticleOncotarget2016
Inflammaging increases susceptibility to cigarette smoke-induced COPD.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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.
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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
41 citing papers in PubMed, 50 citations in OpenAlex.
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- Targeting immunosenescence in lung diseases: mechanistic insights and clinical interventions.BMC medicine · 2026Review
- B cells and iBALT in TB immunity & pathogenesis.Frontiers in immunology · 2026Review
- Impact of intranasal cigarette smoke exposure on murine peripheral immune responses and lung pathology.Frontiers in toxicology · 2026Article
- Azithromycin Mitigates Tobacco Smoke-Induced Lung Senescence by Modulating the FOXO3A/CCND1 Signaling Pathway.International journal of chronic obstructive pulmonary disease · 2025Article
- Interpretable machine learning uncovers epithelial transcriptional rewiring and a role for Gelsolin in COPD.JCI insight · 2024Article
- Unveiling mechanisms of lung aging in COPD: A promising target for therapeutics development.Chinese medical journal pulmonary and critical care medicine · 2024Review
- Immunosenescence and Inflammation in Chronic Obstructive Pulmonary Disease: A Systematic Review.Journal of clinical medicine · 2024Review
- Age-Dependent Inflammatory Microenvironment Mediates Alveolar Regeneration.International journal of molecular sciences · 2024Article
- Contribution of adaptive immunity to human COPD and experimental models of emphysema.Physiological reviews · 2023Review
- Article
- P16INK4A-More Than a Senescence Marker.Life (Basel, Switzerland) · 2022Review
- Cellular Senescence in Aging Lungs and Diseases.Cells · 2022Review
- Lung emphysema and impaired macrophage elastase clearance in mucolipin 3 deficient mice.Nature communications · 2022Article
- Review
- The Role of Extracellular Vesicles as a Shared Disease Mechanism Contributing to Multimorbidity in Patients With COPD.Frontiers in immunology · 2021Review
- Article
- Single cell and tissue-transcriptomic analysis of murine bladders reveals age- and TNFα-dependent but microbiota-independent tertiary lymphoid tissue formation.Mucosal immunology · 2020Article
- Lung regeneration: implications of the diseased niche and ageing.European respiratory review : an official journal of the European Respiratory Society · 2020Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic obstructive pulmonary disease (COPD) is related to an abnormal chronic inflammatory response of the lung to mainly cigarette smoke (CS) and the disease risk is increased in aged individuals. The source of this chronic inflammation is due to the repeated and progressive activation of immune cells. We hypothesize that in a chronic CS-induced mouse model, the predisposition to COPD pathogenesis in aged mice is characterized by an elevated immune response compared to young animals. We measured several characteristics of COPD in young and old mice (2 and 12 months of age) exposed to CS for 3 months. CS-exposed aged mice exhibited increased lung compliance (0.061 ± 0.008 vs. 0.055 ± 0.006 ml/cm H2O, p < 0.01), emphysema development (35.36 ± 0.71 vs. 25.31 ± 0.005 μm; p < 0.01) and airway remodeling (2.15 ± 0.37 vs. 1.09 ± 0.64 μm3/μm2; p < 0.01) compared to control animals, which was not seen in CS-exposed young mice. Quantification of lung tissue inflammation revealed a significantly greater volume of inducible bronchus-associated lymphoid tissue structures in aged mice after CS exposure (5.94 ± 2.89 vs. 2.37 ± 1.69 μm3/μm2; p < 0.01). Our results indicate that age-induced lung inflammation is further elevated after CS exposure in old mice, potentially via an age-induced change in immune cell susceptibility to CS thereby accelerating the pathophysiological hallmarks of COPD.
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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.