ArticleNature communications2015
Matrikines are key regulators in modulating the amplitude of lung inflammation in acute pulmonary infection.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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
42 citing papers in PubMed, 64 citations in OpenAlex.
- Identification and characterization of a Fibrillin-1 derived matrikine for cardiac regeneration and repair.Biomaterials · 2026Article
- An update on the landscape of collagen bioactive fragments.The FEBS journal · 2026Review
- Diabetes Mellitus Facilitates Gallstone Formation Through CXCR2-NETs-Mediated Liver-Bile Barrier Damage.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The Extracellular Matrix and the Immune System in Acute Lung Injury: Partners in Damage and Repair.Biomedicines · 2025Review
- Identification and characterization of a Fibrillin-1 derived matrikine for cardiac regeneration and repair.bioRxiv : the preprint server for biology · 2025Article
- Advances in Designer Materials for Chronic Wound Healing.Advances in wound care · 2025Review
- The LTB4-BLT1 axis attenuates influenza-induced lung inflammation by suppressing NLRP3 activation.Cell death discovery · 2025Article
- A lactobacilli-based inhaled live biotherapeutic product attenuates pulmonary neutrophilic inflammation.Nature communications · 2024Article
- A pathological joint-liver axis mediated by matrikine-activated CD4Signal transduction and targeted therapy · 2024Article
- Role of platelet factor 4 in arteriovenous fistula maturation failure: What do we know so far?The journal of vascular access · 2024Review
- Unveiling the immunomodulator role of plasma oxidized lipids in SA-AKI progression: a CRRT perspective.Frontiers in physiology · 2024Article
- Relationship BetweenOpen forum infectious diseases · 2023Article
- The role of infected epithelial cells inFrontiers in cellular and infection microbiology · 2023Review
- The extracellular microenvironment in immune dysregulation and inflammation in retinal disorders.Frontiers in immunology · 2023Review
- Neutrophil Recruitment in Pneumococcal Pneumonia.Frontiers in cellular and infection microbiology · 2022Review
- An immunodominant NPNature immunology · 2022Article
- Current Status of the Use of Multifunctional Enzymes as Anti-Cancer Drug Targets.Pharmaceutics · 2021Review
- Pulmonary delivery of the broad-spectrum matrix metalloproteinase inhibitor marimastat diminishes multiwalled carbon nanotube-induced circulating bioactivity without reducing pulmonary inflammation.Particle and fibre toxicology · 2021Article
- Article
- Regulatory mechanisms of neutrophil migration from the circulation to the airspace.Cellular and molecular life sciences : CMLS · 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
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Bioactive matrix fragments (matrikines) have been identified in a myriad of disorders, but their impact on the evolution of airway inflammation has not been demonstrated. We recently described a pathway where the matrikine and neutrophil chemoattractant proline-glycine-proline (PGP) could be degraded by the enzyme leukotriene A4 hydrolase (LTA4H). LTA4H classically functions in the generation of pro-inflammatory leukotriene B4, thus LTA4H exhibits opposing pro- and anti-inflammatory activities. The physiological significance of this secondary anti-inflammatory activity remains unknown. Here we show, using readily resolving pulmonary inflammation models, that loss of this secondary activity leads to more pronounced and sustained inflammation and illness owing to PGP accumulation. PGP elicits an exacerbated neutrophilic inflammation and protease imbalance that further degrades the extracellular matrix, generating fragments that perpetuate inflammation. This highlights a critical role for the secondary anti-inflammatory activity of LTA4H and thus has consequences for the generation of global LTA4H inhibitors currently being developed.
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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.