ArticleAmerican journal of respiratory cell and molecular biology2019
Cigarette Smoke Triggers IL-33-associated Inflammation in a Model of Late-Stage Chronic Obstructive Pulmonary Disease.
Article in American journal of respiratory cell and molecular biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 29 citations in OpenAlex.
- A Synthetic Lethality-Informed Multi-Omic Framework for Identifying a Five-Gene Diagnostic Signature in Chronic Obstructive Pulmonary Disease.Current issues in molecular biology · 2026Article
- Emerging Systemic Treatments for Asthma and Allergic Diseases: New Tricks, Same Dog?The journal of allergy and clinical immunology. In practice · 2026Review
- The predictive value of combined detection of serum IL-33, TSLP and eosinophils in the treatment effect and exacerbation risk of chronic obstructive pulmonary disease.BMC pulmonary medicine · 2026Article
- ILC2 Diversity, Location, and Function in Pulmonary Disease.Immunological reviews · 2025Review
- Targeting alarmins in asthma: From bench to clinic.The Journal of allergy and clinical immunology · 2025Review
- Cigarette Smoking Induces Skeletal Muscle Atrophy in Mice by Activated Macrophage-Mediated Pyroptosis.Journal of inflammation research · 2025Article
- Identifying the Key Mitochondria-Related Genes in COPD by Integrating Machine Learning and Bioinformatics Analyses.International journal of genomics · 2025Article
- IL-33 as a biomarker for disease severity in COPD with lung cancer comorbidity.American journal of cancer research · 2025Article
- Cigarette smoke exposure impairs early-stage recovery from lengthening contraction-induced muscle injury in male mice.Physiological reports · 2024Article
- GC/HRMS Analysis of E-Liquids Complements In Vivo Modeling Methods and can Help to Predict Toxicity.ACS omega · 2024Article
- Activator protein transcription factors coordinate human IL-33 expression from noncanonical promoters in chronic airway disease.JCI insight · 2024Article
- Interplay of IL-33 and IL-35 Modulates Th2/Th17 Responses in Cigarette Smoke Exposure HDM-Induced Asthma.Inflammation · 2024Article
- The production, function, and clinical applications of IL-33 in type 2 inflammation-related respiratory diseases.Frontiers in immunology · 2024Review
- Role of IL-33-ST2 pathway in regulating inflammation: current evidence and future perspectives.Journal of translational medicine · 2023Review
- Pathophysiology and pathogenic mechanisms of pulmonary hypertension: role of membrane receptors, ion channels, and CaPhysiological reviews · 2023Review
- IL-33/ST2 receptor-dependent signaling in the development of pulmonary hypertension in Sugen/hypoxia mice.Physiological reports · 2022Article
- Loss of IL-33 enhances elastase-induced and cigarette smoke extract-induced emphysema in mice.Respiratory research · 2021Article
- Update in Chronic Obstructive Pulmonary Disease 2019.American journal of respiratory and critical care medicine · 2020Review
- IL-33 Mediates Lung Inflammation by the IL-6-Type Cytokine Oncostatin M.Mediators of inflammation · 2020Article
- Linking VEGF Deficiency and IL-33 Upregulation in Chronic Obstructive Pulmonary Disease.American journal of respiratory cell and molecular biology · 2019Article
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6 authors at 1 institution in 1 country.
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Abstract
Chronic obstructive pulmonary disease (COPD) is a worldwide threat. Cigarette smoke (CS) exposure causes cardiopulmonary disease and COPD and increases the risk for pulmonary tumors. In addition to poor lung function, patients with COPD are susceptible to bouts of dangerous inflammation triggered by pollutants or infection. These severe inflammatory episodes can lead to additional exacerbations, hospitalization, further deterioration of lung function, and reduced survival. Suitable models of the inflammatory conditions associated with CS, which potentiate the downward spiral in patients with COPD, are lacking, and the underlying mechanisms that trigger exacerbations are not well understood. Although initial CS exposure activates a protective role for vascular endothelial growth factor (VEGF) functions in barrier integrity, chronic exposure depletes the pulmonary VEGF guard function in severe COPD. Thus, we hypothesized that mice with compromised VEGF production and challenged with CS would trigger human-like severe inflammatory progression of COPD. In this model, we discovered that CS exposure promotes an amplified IL-33 cytokine response and severe disease progression. Our
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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.