ArticleAmerican journal of physiology. Lung cellular and molecular physiology2009
Cigarette smoke-induced emphysema in A/J mice is associated with pulmonary oxidative stress, apoptosis of lung cells, and global alterations in gene expression.
Article in American journal of physiology. Lung cellular and molecular physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
75 citing papers in PubMed, 128 citations in OpenAlex.
- Compartmentalization of anti-oxidant and anti-inflammatory gene expression in current and former smokers with COPD.Respiratory research · 2019Trial
- Systematic cell-type resolved transcriptomes of 8 tissues in 8 lab and wild-derived mouse strains capture global and local expression variation.Cell genomics · 2026Article
- Blocking IL-23 Signaling Mitigates Cigarette Smoke-Induced Murine Emphysema.Environmental toxicology · 2024Article
- Differences in Airway Remodeling and Emphysematous Lesions between Rats Exposed to Smoke from New-Type and Conventional Tobacco Varieties.Antioxidants (Basel, Switzerland) · 2024Article
- An update in club cell biology and its potential relevance to chronic obstructive pulmonary disease.American journal of physiology. Lung cellular and molecular physiology · 2023Review
- Single-Walled vs. Multi-Walled Carbon Nanotubes: Influence of Physico-Chemical Properties on Toxicogenomics Responses in Mouse Lungs.Nanomaterials (Basel, Switzerland) · 2023Article
- Dysregulated Polycomb Repressive Complex 2 contributes to chronic obstructive pulmonary disease by rewiring stem cell fate.Stem cell reports · 2023Article
- Nebulization of risedronate alleviates airway obstruction and inflammation of chronic obstructive pulmonary diseases via suppressing prenylation-dependent RAS/ERK/NF-κB and RhoA/ROCK1/MLCP signaling.Respiratory research · 2022Article
- Role of Nuclear Factor Erythroid 2‒Related Factor 2 in Chronic Obstructive Pulmonary Disease.Tuberculosis and respiratory diseases · 2022Review
- Early life exposure to nicotine modifies lung gene response after elastase-induced emphysema.Respiratory research · 2022Article
- Effect of pirfenidone protecting against cigarette smoke extract induced apoptosis.Tobacco induced diseases · 2022Article
- Impact of whole-body versus nose-only inhalation exposure systems on systemic, respiratory, and cardiovascular endpoints in a 2-month cigarette smoke exposure study in the ApoEJournal of applied toxicology : JAT · 2021Article
- A 6-month inhalation toxicology study in ApoeArchives of toxicology · 2021Article
- Single cell RNA sequencing identifies IGFBP5 and QKI as ciliated epithelial cell genes associated with severe COPD.Respiratory research · 2021Article
- Loss of Endothelial WWOX: A Risk Factor for ARDS in Smokers?American journal of respiratory cell and molecular biology · 2021Article
- The Heterogeneity of Inflammatory Response and Emphysema in Chronic Obstructive Pulmonary Disease.Frontiers in physiology · 2021Article
- Cigarette Smoke Triggers IL-33-associated Inflammation in a Model of Late-Stage Chronic Obstructive Pulmonary Disease.American journal of respiratory cell and molecular biology · 2019Article
- Identification of Putative Regulatory Alterations Leading to Changes in Gene Expression in Chronic Obstructive Pulmonary Disease.Molecules and cells · 2019Article
- Health risk of metal exposure via inhalation of cigarette sidestream smoke particulate matter.Environmental science and pollution research international · 2019Article
- Therapeutic targeting of the NRF2 and KEAP1 partnership in chronic diseases.Nature reviews. Drug discovery · 2019Review
15 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Cigarette smoking is the major risk factor for developing chronic obstructive pulmonary disease, the fourth leading cause of deaths in the United States. Despite recent advances, the molecular mechanisms involved in the initiation and progression of this disease remain elusive. We used Affymetrix Gene Chip arrays to determine the temporal alterations in global gene expression during the progression of pulmonary emphysema in A/J mice. Chronic cigarette smoke (CS) exposure caused pulmonary emphysema in A/J mice, which was associated with pronounced bronchoalveolar inflammation, enhanced oxidative stress, and increased apoptosis of alveolar septal cells. Microarray analysis revealed the upregulation of 1,190, 715, 260, and 246 genes and the downregulation of 1,840, 730, 442, and 236 genes in the lungs of mice exposed to CS for 5 h, 8 days, and 1.5 and 6 mo, respectively. Most of the genes belong to the functional categories of phase I genes, Nrf2-regulated antioxidant and phase II genes, phase III detoxification genes, and others including immune/inflammatory response genes. Induction of the genes encoding multiple phase I enzymes was markedly higher in the emphysematous lungs, whereas reduced expression of various cytoprotective genes constituting ubiquitin-proteasome complex, cell survival pathways, solute carriers and transporters, transcription factors, and Nrf2-regulated antioxidant and phase II-responsive genes was noted. Our data indicate that the progression of CS-induced emphysema is associated with a steady decline in the expression of various genes involved in multiple pathways in the lungs of A/J mice. Many of the genes discovered in this study could rationally play an important role in the susceptibility to CS-induced emphysema.
Indexed as
Identifiers
What OpenQuestion holds
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.