ArticleFrontiers in cell and developmental biology2018
Progression of Pulmonary Emphysema and Continued Increase in Ectodomain Shedding of Cell Adhesion Molecule 1 After Cessation of Cigarette Smoke Exposure in Mice.
Article in Frontiers in cell and developmental biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 7 citations in OpenAlex.
- A titratable murine model of progressive emphysema using tracheal porcine pancreatic elastase.Scientific reports · 2023Article
- Proteomic Network Analysis of Bronchoalveolar Lavage Fluid in Ex-Smokers to Discover Implicated Protein Targets and Novel Drug Treatments for Chronic Obstructive Pulmonary Disease.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Paraseptal Emphysema: From the Periphery of the Lobule to the Center of the Stage.American journal of respiratory and critical care medicine · 2020Article
- Long-Term Sequelae of Smoking and Cessation in Spontaneously Hypertensive Rats.Toxicologic pathology · 2020Article
- Adipose Tissue-Derived Stem Cells Have the Ability to Differentiate into Alveolar Epithelial Cells and Ameliorate Lung Injury Caused by Elastase-Induced Emphysema in Mice.Stem cells international · 2019Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pulmonary emphysema usually arises in cigarette smokers, and often progresses after smoking cessation and even in ex-smokers. Lung-epithelial cell adhesion molecule 1 (CADM1), an immunoglobulin superfamily member, is extracellularly shed to produce a proapoptotic C-terminal fragment (CTF) within the cell and contribute to the development of emphysema. Here, we made an ex-smoker model using C57BL/6 mice; mice (6-week-old; 5 mice per group) were exposed to passive smoke of eight cigarettes twice a day 5 days a week until 18 weeks of age, and were then left untreated until 30 weeks of age. We calculated the mean linear intercept (Lm) and the alveolar septal thickness in the lung histologic sections to estimate the alveolar space dilatation. At 18 weeks of age, Lm was marginally enlarged (
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Registered trials
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