ReviewFrontiers in immunology2023
Dipeptidyl peptidase 1 inhibition as a potential therapeutic approach in neutrophil-mediated inflammatory disease.
Review in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- Efficacy and safety of DPP-1 inhibitors in bronchiectasis: a GRADE-assessed meta-analysis of randomized controlled trials.Respiratory research · 2025Pooled it
- Proteomic changes induced by acute exercise and high-intensity interval training during pregnancy: a pilot randomised controlled trial.Scientific reports · 2025Trial
- Safety, tolerability, pharmacokinetics and pharmacodynamics of HSK31858, a novel oral dipeptidyl peptidase-1 inhibitor, in healthy volunteers: An integrated phase 1, randomized, double-blind, placebo-controlled, single- and multiple-ascending dose study.British journal of clinical pharmacology · 2025Trial
- Neutrophils: The Overlooked Regenerative Role in Bone Repair.Stem cell reviews and reports · 2026Review
- The dipeptidyl peptidase 1 inhibition landscape in bronchiectasis and its future direction.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Targeting Cathepsin C in Cancer Metastasis: Protease Network Activation, Inflammatory Crosstalk, and Therapeutic Opportunities.International journal of molecular sciences · 2026Review
- Review
- Nitrogen-containing FDA-approved drugs in 2025: synthesis, significance and therapeutic applications.RSC advances · 2026Review
- Crosstalk between circulating DPP3 and immune cells in the context of cardio-systemic stress.iScience · 2026Article
- Brensocatib-Another Therapeutic "Window of Opportunity" for Patients with Bronchiectasis.Journal of clinical medicine · 2026Review
- Brensocatib: First Approval.Drugs · 2026Review
- Impact of dipeptidyl peptidase I and neutrophil serine proteases on neutrophil functional responses.Frontiers in pharmacology · 2026Article
- Tackling Neutrophilic Inflammation in Bronchiectasis: From Macrolides to Cathepsin C Inhibitors.Journal of inflammation research · 2026Review
- 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
- Cathepsin C-driven enhancement of neutrophil extracellular trap formation contributes to acute lung injury.iScience · 2025Article
- A Novel Role of Neutrophil Elastase in Podocyte Dysfunction Induced by High Glucose, PMA, and MDP.Journal of cellular physiology · 2025Article
- Protective effects of neutrophil serine protease inhibition against ischemia-reperfusion injury in lung or heart transplantation.The FEBS journal · 2025Review
- Making real progress in the world of bronchiectasis.Journal of thoracic disease · 2025Article
- Mast Cells Are Not Essential for Pubertal Mammary Gland Branching.European journal of immunology · 2025Article
- Dipeptidyl peptidase 1 inhibitors and neutrophilic inflammation in bronchiectasis: a narrative review.Journal of thoracic disease · 2025Review
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 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neutrophils have a critical role in the innate immune response to infection and the control of inflammation. A key component of this process is the release of neutrophil serine proteases (NSPs), primarily neutrophil elastase, proteinase 3, cathepsin G, and NSP4, which have essential functions in immune modulation and tissue repair following injury. Normally, NSP activity is controlled and modulated by endogenous antiproteases. However, disruption of this homeostatic relationship can cause diseases in which neutrophilic inflammation is central to the pathology, such as chronic obstructive pulmonary disease (COPD), alpha-1 antitrypsin deficiency, bronchiectasis, and cystic fibrosis, as well as many non-pulmonary pathologies. Although the pathobiology of these diseases varies, evidence indicates that excessive NSP activity is common and a principal mediator of tissue damage and clinical decline. NSPs are synthesized as inactive zymogens and activated primarily by the ubiquitous enzyme dipeptidyl peptidase 1, also known as cathepsin C. Preclinical data confirm that inactivation of this protease reduces activation of NSPs. Thus, pharmacological inhibition of dipeptidyl peptidase 1 potentially reduces the contribution of aberrant NSP activity to the severity and/or progression of multiple inflammatory diseases. Initial clinical data support this view. Ongoing research continues to explore the role of NSP activation by dipeptidyl peptidase 1 in different disease states and the potential clinical benefits of dipeptidyl peptidase 1 inhibition.
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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.