ArticleAmerican journal of physiology. Lung cellular and molecular physiology2015
Airway epithelial cell PPARγ modulates cigarette smoke-induced chemokine expression and emphysema susceptibility in mice.
Article in American journal of physiology. Lung cellular and molecular physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
What it found
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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
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.
- Genetic variations in anti-diabetic drug targets and COPD risk: evidence from mendelian randomization.BMC pulmonary medicine · 2024Pooled it
- Regenerative therapeutics for chronic obstructive pulmonary disease.Pharmacological reviews · 2026Review
- The Inflammatory Roles of n-3 and n-6 Polyunsaturated Fatty Acids in COPD: Clinical Implications and Underlying Mechanisms.Journal of inflammation research · 2026Review
- Post-COPD: Can Emphysema Be Repaired?American journal of respiratory and critical care medicine · 2025Article
- ATF1 and miR-27b-3p drive intervertebral disc degeneration through the PPARG/NF-κB signaling axis.Communications biology · 2025Article
- Proteogenomic verifies targets underlying erythromycin alleviate neutrophil extracellular traps-induced inflammation.Respiratory research · 2025Article
- Bioinformatic Insights and XGBoost Identify Shared Genetics in Chronic Obstructive Pulmonary Disease and Type 2 Diabetes.The clinical respiratory journal · 2025Article
- Article
- Mesenchymal stromal cells reduce inflammation and improve lung function in a mouse model of cystic fibrosis lung disease.Scientific reports · 2024Article
- B cell-derived IL-10 promotes the resolution of lipopolysaccharide-induced acute lung injury.Cell death & disease · 2023Article
- Low 15d-PGJ2 status is associated with oxidative stress in chronic obstructive pulmonary disease patients.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- Systemic and Airway Epigenetic Disruptions Are Associated with Health Status in COPD.Biomedicines · 2023Article
- Modulation of mouse laryngeal inflammatory and immune cell responses by low and high doses of mainstream cigarette smoke.Scientific reports · 2022Article
- Insight into the pulmonary molecular toxicity of heated tobacco products using human bronchial and alveolar mucosa models at air-liquid interface.Scientific reports · 2022Article
- Review
- Role of specialized pro-resolving lipid mediators in pulmonary inflammation diseases: mechanisms and development.Respiratory research · 2021Review
- Integration of transcriptome analysis with pathophysiological endpoints to evaluate cigarette smoke toxicity in an in vitro human airway tissue model.Archives of toxicology · 2021Article
- Biotite-Calx Based Traditional Indian MedicineJournal of inflammation research · 2021Article
- 16HBE Cell Lipid Mediator Responses to Mono and Co-Infections with Respiratory Pathogens.Metabolites · 2020Article
- Effects of cannabis oil extract on immune response gene expression in human small airway epithelial cells (HSAEpC): implications for chronic obstructive pulmonary disease (COPD).Journal of cannabis research · 2020Article
Corrections and comments
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Authors and funding
11 authors at 7 institutions in 2 countries.
Funding
Abstract
Chronic obstructive pulmonary disease (COPD) is a highly prevalent, chronic inflammatory lung disease with limited existing therapeutic options. While modulation of peroxisome proliferator-activating receptor (PPAR)-γ activity can modify inflammatory responses in several models of lung injury, the relevance of the PPARG pathway in COPD pathogenesis has not been previously explored. Mice lacking Pparg specifically in airway epithelial cells displayed increased susceptibility to chronic cigarette smoke (CS)-induced emphysema, with excessive macrophage accumulation associated with increased expression of chemokines, Ccl5, Cxcl10, and Cxcl15. Conversely, treatment of mice with a pharmacological PPARγ activator attenuated Cxcl10 and Cxcl15 expression and macrophage accumulation in response to CS. In vitro, CS increased lung epithelial cell chemokine expression in a PPARγ activation-dependent fashion. The ability of PPARγ to regulate CS-induced chemokine expression in vitro was not specifically associated with peroxisome proliferator response element (PPRE)-mediated transactivation activity but was correlated with PPARγ-mediated transrepression of NF-κB activity. Pharmacological or genetic activation of PPARγ activity abrogated CS-dependent induction of NF-κB activity. Regulation of NF-κB activity involved direct PPARγ-NF-κB interaction and PPARγ-mediated effects on IKK activation, IκBα degradation, and nuclear translocation of p65. Our data indicate that PPARG represents a disease-relevant pathophysiological and pharmacological target in COPD. Its activation state likely contributes to NF-κB-dependent, CS-induced chemokine-mediated regulation of inflammatory cell accumulation.
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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.