ArticlePloS one2015
Repression of CC16 by cigarette smoke (CS) exposure.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 54 citations in OpenAlex.
- Short halt in vaping modifies cardiorespiratory parameters and urine metabolome: a randomized trial.American journal of physiology. Lung cellular and molecular physiology · 2020Trial
- From respiratory infections to environmental exposures: CC16 is a key modulator of airway homeostasis.Frontiers in medicine · 2026Review
- Identification ofFrontiers in immunology · 2026Review
- rhCC16 Suppresses Cellular Senescence and Ameliorates COPD-Like Symptoms by Activating the AMPK/Sirt1-PGC-1-α-TFAM Pathway to Promote Mitochondrial Function.Journal of cellular and molecular medicine · 2025Article
- Controlled human exposures: a review and comparison of the health effects of diesel exhaust and wood smoke.Particle and fibre toxicology · 2024Review
- Club cell protein (CC16) in serum as an effect marker for small airway epithelial damage caused by diesel exhaust and blasting fumes in potash mining.International archives of occupational and environmental health · 2024Article
- Article
- CC16 as an Inflammatory Biomarker in Induced Sputum Reflects Chronic Obstructive Pulmonary Disease (COPD) Severity.International journal of chronic obstructive pulmonary disease · 2023Article
- Relationships of serum CC16 levels with smoking status and lung function in COPD.Respiratory research · 2022Article
- Vitamin D3 alleviates cigarette smoke extract-mediated epithelial-mesenchymal transition and fibrogenesis by upregulating CC16 expression in bronchial epithelial cells.Experimental and therapeutic medicine · 2022Article
- Pathogenesis of chronic obstructive pulmonary disease: understanding the contributions of gene-environment interactions across the lifespan.The Lancet. Respiratory medicine · 2022Review
- Lung developmental is altered after inhalation exposure to various concentrations of calcium arsenate.Toxicology and applied pharmacology · 2021Article
- Article
- Club Cell Secreted Protein CC16: Potential Applications in Prognosis and Therapy for Pulmonary Diseases.Journal of clinical medicine · 2020Review
- Stem cells and lung regeneration.American journal of physiology. Cell physiology · 2020Review
- Differential expression of lung adenocarcinoma transcriptome with signature of tobacco exposure.Journal of applied genetics · 2020Article
- MUC1 contributes to goblet cell metaplasia and MUC5AC expression in response to cigarette smoke in vivo.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Lung Secretoglobin Scgb1a1 Influences Alveolar Macrophage-Mediated Inflammation and Immunity.Frontiers in immunology · 2020Article
- Reduced Serum Concentration of CC16 Is Associated with Severity of Chronic Obstructive Pulmonary Disease and Contributes to the Diagnosis and Assessment of the Disease.International journal of chronic obstructive pulmonary disease · 2020Observational
- Consecutive Hypoxia Decreases Expression ofFrontiers in cell and developmental biology · 2020Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Club (Clara) Cell Secretory Protein (CCSP, or CC16) is produced mainly by non-ciliated airway epithelial cells including bronchiolar club cells and the change of its expression has been shown to associate with the progress and severity of Chronic Obstructive Pulmonary Disease (COPD). In an animal model, the lack of CC16 renders the animal susceptible to the tumorigenic effect of a major CS carcinogen. A recent population-based Tucson Epidemiological Study of Airway Obstructive Diseases (TESAOD) has indicated that the low serum CC16 concentration is closely linked with the smoke-related mortality, particularly that driven by the lung cancer. However, the study of CC16 expression in well-defined smoke exposure models has been lacking, and there is no experimental support for the potential causal link between CC16 and CS-induced pathophysiological changes in the lung. In the present study, we have found that airway CC16 expression was significantly repressed in COPD patients, in monkey CS exposure model, and in CS-induced mouse model of COPD. Additionally, the lack of CC16 exacerbated airway inflammation and alveolar loss in the mouse model. Therefore, CC16 may play an important protective role in CS-related diseases.
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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.