ReviewRespiratory research2018
Proteinase 3; a potential target in chronic obstructive pulmonary disease and other chronic inflammatory diseases.
Review in Respiratory research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 53 citations in OpenAlex.
- The convergent pathway of obstructive lung disease: the disease-modifying potential of dipeptidyl peptidase 1 inhibition in COPD, asthma and bronchiectasis overlap.Drugs in context · 2026Review
- Observational
- Neutrophilic Asthma-From Mechanisms to New Perspectives of Therapy.Journal of clinical medicine · 2025Review
- Exploring the involvement of serine proteases in neutrophil extracellular traps: a review of mechanisms and implications.Cell death & disease · 2025Review
- Dipeptidyl peptidase-1 inhibitors in bronchiectasis.European respiratory review : an official journal of the European Respiratory Society · 2025Review
- Expression and purification of human neutrophil proteinase 3 from insect cells and characterization of ligand binding.PloS one · 2024Article
- The association between pan-immune-inflammation value and chronic obstructive pulmonary disease: data from NHANES 1999-2018.Frontiers in physiology · 2024Article
- Study on Potential Differentially Expressed Genes in Idiopathic Pulmonary Fibrosis by Bioinformatics and Next-Generation Sequencing Data Analysis.Biomedicines · 2023Article
- The prevalence of bronchiectasis in patients with alpha-1 antitrypsin deficiency: initial report of EARCO.Orphanet journal of rare diseases · 2023Article
- Dipeptidyl peptidase 1 inhibition as a potential therapeutic approach in neutrophil-mediated inflammatory disease.Frontiers in immunology · 2023Review
- Review
- Roles of neutrophil granule proteins in orchestrating inflammation and immunity.The FEBS journal · 2022Review
- Predicting the pulmonary effects of long-term e-cigarette use: are the clouds clearing?European respiratory review : an official journal of the European Respiratory Society · 2022Review
- Targeting Neutrophils for Promoting the Resolution of Inflammation.Frontiers in immunology · 2022Review
- Protease-Antiprotease Imbalance in Bronchiectasis.International journal of molecular sciences · 2021Review
- Review
- Pathogenesis and pathology of anti-neutrophil cytoplasmic antibody（ANCA）-associated vasculitis.Journal of translational autoimmunity · 2021Review
- Exacerbations of Lung Disease in Alpha-1 Antitrypsin Deficiency.Chronic obstructive pulmonary diseases (Miami, Fla.) · 2021Article
- Pathogenicity of Proteinase 3-Anti-Neutrophil Cytoplasmic Antibody in Granulomatosis With Polyangiitis: Implications as Biomarker and Future Therapies.Frontiers in immunology · 2021Review
- Peptidyl Activity-Based Probes for Imaging Serine Proteases.Frontiers in chemistry · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic Obstructive Pulmonary Disease (COPD) is a common, multifactorial lung disease which results in significant impairment of patients' health and a large impact on society and health care burden. It is believed to be the result of prolonged, destructive neutrophilic inflammation which results in progressive damage to lung structures. During this process, large quantities of neutrophil serine proteinases (NSPs) are released which initiate the damage and contribute towards driving a persistent inflammatory state.Neutrophil elastase has long been considered the key NSP involved in the pathophysiology of COPD. However, in recent years, a significant role for Proteinase 3 (PR3) in disease development has emerged, both in COPD and other chronic inflammatory conditions. Therefore, there is a need to investigate the importance of PR3 in disease development and hence its potential as a therapeutic target. Research into PR3 has largely been confined to its role as an autoantigen, but PR3 is involved in triggering inflammatory pathways, disrupting cellular signalling, degrading key structural proteins, and pathogen response.This review summarises what is presently known about PR3, explores its involvement particularly in the development of COPD, and indicates areas requiring further investigation.
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.