ArticleJCI insight2023
CC16 augmentation reduces exaggerated COPD-like disease in Cc16-deficient mice.
Article in JCI insight, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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.
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
12 citing papers in PubMed, 12 citations in OpenAlex.
- Pharmacological effect of rhCC16 on COPD: anti-senescence via the PI3K-AKT-mTOR pathway.Molecular and cellular biochemistry · 2026Article
- Maternal smoking and CC-16: implications for lung development and COPD across the lifespan.American journal of respiratory and critical care medicine · 2026Article
- From respiratory infections to environmental exposures: CC16 is a key modulator of airway homeostasis.Frontiers in medicine · 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
- Clara cell 10 (CC10) protein attenuates allergic airway inflammation by modulating lung dendritic cell functions.Cellular and molecular life sciences : CMLS · 2024Article
- txci-ATAC-seq: a massive-scale single-cell technique to profile chromatin accessibility.Genome biology · 2024Article
- Protection against cigarette smoke-induced chronic obstructive pulmonary disease via activation of the SIRT1/FoxO1 axis by targeting microRNA-132.American journal of translational research · 2024Article
- Botanical formulation HX110B ameliorates PPE-induced emphysema in mice via regulation of PPAR/RXR signaling pathway.PloS one · 2024Article
- Sputum Biomarkers in Wood and Tobacco Smoke Etiotypes of Chronic Obstructive Pulmonary Disease.International journal of chronic obstructive pulmonary disease · 2024Article
- Deciphering NF-kappaB pathways in smoking-related lung carcinogenesis.EXCLI journal · 2024Review
- Article
- CC16 drives VLA-2-dependent SPLUNC1 expression.Frontiers in immunology · 2023Article
Corrections and comments
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Authors and funding
16 authors at 3 institutions in 2 countries.
Funding
Abstract
Low Club Cell 16 kDa protein (CC16) plasma levels are linked to accelerated lung function decline in patients with chronic obstructive pulmonary disease (COPD). Cigarette smoke-exposed (CS-exposed) Cc16-/- mice have exaggerated COPD-like disease associated with increased NF-κB activation in their lungs. It is unclear whether CC16 augmentation can reverse exaggerated COPD in CS-exposed Cc16-/- mice and whether increased NF-κB activation contributes to the exaggerated COPD in CS-exposed Cc16-/- lungs. CS-exposed WT and Cc16-/- mice were treated with recombinant human CC16 (rhCC16) or an NF-κB inhibitor versus vehicle beginning at the midpoint of the exposures. COPD-like disease and NF-κB activation were measured in the lungs. RhCC16 limited the progression of emphysema, small airway fibrosis, and chronic bronchitis-like disease in WT and Cc16-/- mice partly by reducing pulmonary inflammation (reducing myeloid leukocytes and/or increasing regulatory T and/or B cells) and alveolar septal cell apoptosis, reducing NF-κB activation in CS-exposed Cc16-/- lungs, and rescuing the reduced Foxj1 expression in CS-exposed Cc16-/- lungs. IMD0354 treatment reduced exaggerated lung inflammation and rescued the reduced Foxj1 expression in CS-exposed Cc16-/- mice. RhCC16 treatment reduced NF-κB activation in luciferase reporter A549 cells. Thus, rhCC16 treatment limits COPD progression in CS-exposed Cc16-/- mice partly by inhibiting NF-κB activation and represents a potentially novel therapeutic approach for 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.