ReviewChinese medical journal2017
Role of Neutrophil Extracellular Traps in Asthma and Chronic Obstructive Pulmonary Disease.
Review in Chinese medical journal, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.
- Characteristics and Role of Neutrophil Extracellular Traps in Asthma.Inflammation · 2022Pooled it
- Cell death crosstalk in NET-Driven inflammation: mechanisms, disease contexts, and therapeutic perspectives.Biomarker research · 2026Review
- Neutrophil Plasticity in Airway Disease: Balancing Damage and Repair.Journal of innate immunity · 2026Review
- Nitric oxide synthase inhibitors reduce the formation of neutrophil extracellular traps and alleviate airway inflammation in the mice model of asthma.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Pathogenic Cell in COPD: Mechanisms of Airway Remodeling, Immune Dysregulation, and Therapeutic Implications.International journal of chronic obstructive pulmonary disease · 2025Review
- The role of innate immune system in respiratory viral infection related asthma.Frontiers in cellular and infection microbiology · 2025Review
- Article
- Airway mucus in pulmonary diseases: Muco-adhesive and muco-penetrating particles to overcome the airway mucus barriers.International journal of pharmaceutics · 2023Review
- Asthma-associated bacterial infections: Are they protective or deleterious?The journal of allergy and clinical immunology. Global · 2023Review
- Insights into Personalised Medicine in Bronchiectasis.Journal of personalized medicine · 2023Review
- Serum pro-inflammatory biomarkers associated with improvement in quality of life in pulmonary tuberculosis.Frontiers in immunology · 2023Article
- Review
- Novel potential treatable traits in asthma: Where is the research taking us?The journal of allergy and clinical immunology. Global · 2022Review
- Role of Histone Post-Translational Modifications in Inflammatory Diseases.Frontiers in immunology · 2022Review
- Mechanisms, Pathophysiology and Currently Proposed Treatments of Chronic Obstructive Pulmonary Disease.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Sialic acid-binding immunoglobulin-like lectin 9 as a potential therapeutic target for chronic obstructive pulmonary disease.Chinese medical journal · 2021Article
- CXCL-8-dependent and -independent neutrophil activation in COPD: experiences from a pilot study of the CXCR2 antagonist danirixin.ERJ open research · 2020Article
- The cGAS-STING pathway: The role of self-DNA sensing in inflammatory lung disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Review
- NETs: a new biomarker of traffic-related air pollution exposure: are they ready to catch fish?The European respiratory journal · 2020Article
- Plasma neutrophil extracellular trap level is modified by disease severity and inhaled corticosteroids in chronic inflammatory lung diseases.Scientific reports · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveAsthma and chronic obstructive pulmonary disease (COPD) are representative chronic inflammatory airway diseases responsible for a considerable burden of disease. In this article, we reviewed the relationship between neutrophil extracellular traps (NETs) and chronic inflammatory airway diseases. DATA SOURCES: Articles published up to January 1, 2017, were selected from the PubMed, Ovid Medline, Embase databases, with the keywords of "asthma" or "pulmonary disease, chronic obstructive", "neutrophils" and "extracellular traps." STUDY SELECTION: Articles were obtained and reviewed to analyze the role of NETs in asthma and COPD.
resultsNETs are composed of extracellular DNA, histones, and granular proteins, which are released from activated neutrophils. Multiple studies have indicated that there are a large amount of NETs in the airways of asthmatics and COPD patients. NETs can engulf and kill invading pathogens in the host. However, disordered regulation of NET formation has shown to be involved in the development of asthma and COPD. An overabundance of NETs in the airways or lung tissue could cause varying degrees of damage to lung tissues by inducing the death of human epithelial and endothelial cells, and thus resulting in impairing pulmonary function and accelerating the progress of the disease.
conclusionsExcessive NETs accumulate in the airways of asthmatics and COPD patients. Although NETs play an essential role in the innate immune system against infection, excessive components of NETs can cause lung tissue damage and accelerate disease progression in asthmatics and COPD patients. These findings suggest that administration of NETs could be a novel approach to treat asthma and COPD. Mechanism studies, clinical practice, and strategies to regulate neutrophil activation or directly interrupt NET function in asthmatics and COPD patients are desperately needed.
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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.