ArticleMucosal immunology2016
A pathogenic role for tumor necrosis factor-related apoptosis-inducing ligand in chronic obstructive pulmonary disease.
Article in Mucosal immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
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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
35 citing papers in PubMed, 72 citations in OpenAlex.
- TMEM131-Mediated Soluble TRAIL Triggered Type II Alveolar Epithelial Cell Senescence in Radiation-Induced Lung Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Vitronectin regulates lung tissue remodeling and emphysema in chronic obstructive pulmonary disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Review
- TLR7 promotes smoke-induced experimental lung damage through the activity of mast cell tryptase.Nature communications · 2023Article
- Apoptotic cell death in disease-Current understanding of the NCCD 2023.Cell death and differentiation · 2023Review
- Electronic Cigarette Exposure Increases the Severity of Influenza a Virus Infection via TRAIL Dysregulation in Human Precision-Cut Lung Slices.International journal of molecular sciences · 2023Article
- Airway and parenchyma transcriptomics in a house dust mite model of experimental asthma.Respiratory research · 2023Article
- Novel protein biomarkers for pneumonia and acute exacerbations in COPD: a pilot study.Frontiers in medicine · 2023Article
- TRAIL protects the immature lung from hyperoxic injury.Cell death & disease · 2022Article
- Aim2 suppresses cigarette smoke-induced neutrophil recruitment, neutrophil caspase-1 activation and anti-Ly6G-mediated neutrophil depletion.Immunology and cell biology · 2022Article
- Urine Single-Cell RNA Sequencing in Focal Segmental Glomerulosclerosis Reveals Inflammatory Signatures.Kidney international reports · 2022Article
- Short-term exposure to fine particulate matter and genome-wide DNA methylation in chronic obstructive pulmonary disease: A panel study conducted in Beijing, China.Frontiers in public health · 2022Article
- A Game of Infection - Song of Respiratory Viruses and Interferons.Frontiers in cellular and infection microbiology · 2022Review
- A monoclonal antibody to Siglec-8 suppresses non-allergic airway inflammation and inhibits IgE-independent mast cell activation.Mucosal immunology · 2021Article
- Glomerular Kidney Diseases in the Single-Cell Era.Frontiers in medicine · 2021Review
- Fibulin-1c regulates transforming growth factor-β activation in pulmonary tissue fibrosis.JCI insight · 2019Article
- IL-22 and its receptors are increased in human and experimental COPD and contribute to pathogenesis.The European respiratory journal · 2019Article
- TRAIL signals through the ubiquitin ligase MID1 to promote pulmonary fibrosis.BMC pulmonary medicine · 2019Article
- Roles for T/B lymphocytes and ILC2s in experimental chronic obstructive pulmonary disease.Journal of leukocyte biology · 2019Article
- Ursolic Acid Protected Lung of Rats From Damage Induced by Cigarette Smoke Extract.Frontiers in pharmacology · 2019Article
Corrections and comments
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Authors and funding
19 authors at 5 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic obstructive pulmonary disease (COPD) is a life-threatening inflammatory respiratory disorder, often induced by cigarette smoke (CS) exposure. The development of effective therapies is impaired by a lack of understanding of the underlining mechanisms. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a cytokine with inflammatory and apoptotic properties. We interrogated a mouse model of CS-induced experimental COPD and human tissues to identify a novel role for TRAIL in COPD pathogenesis. CS exposure of wild-type mice increased TRAIL and its receptor messenger RNA (mRNA) expression and protein levels, as well as the number of TRAIL(+)CD11b(+) monocytes in the lung. TRAIL and its receptor mRNA were also increased in human COPD. CS-exposed TRAIL-deficient mice had decreased pulmonary inflammation, pro-inflammatory mediators, emphysema-like alveolar enlargement, and improved lung function. TRAIL-deficient mice also developed spontaneous small airway changes with increased epithelial cell thickness and collagen deposition, independent of CS exposure. Importantly, therapeutic neutralization of TRAIL, after the establishment of early-stage experimental COPD, reduced pulmonary inflammation, emphysema-like alveolar enlargement, and small airway changes. These data provide further evidence for TRAIL being a pivotal inflammatory factor in respiratory diseases, and the first preclinical evidence to suggest that therapeutic agents that target TRAIL may be effective in COPD therapy.
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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.