ReviewThe Yale journal of biology and medicine2012
The effects of extracellular matrix proteins on neutrophil-endothelial interaction--a roadway to multiple therapeutic opportunities.
Review in The Yale journal of biology and medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 22 citations in OpenAlex.
- The role of neutrophils in the pathogenesis of abdominal aortic aneurysms.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Pathophysiological mechanisms and therapeutic potential of E-selectin in pulmonary arterial hypertension.Frontiers in immunology · 2026Review
- Current understanding of the interplay between extracellular matrix remodelling and gut permeability in health and disease.Cell death discovery · 2024Review
- A Serological Neoepitope Biomarker of Neutrophil Elastase-Degraded Calprotectin, Associated with Neutrophil Activity, Identifies Idiopathic Pulmonary Fibrosis and Chronic Obstructive Pulmonary Disease More Effectively Than Total Calprotectin.Journal of clinical medicine · 2023Article
- Radiation-associated secondary malignancies: a novel opportunity for applying immunotherapies.Cancer immunology, immunotherapy : CII · 2023Review
- Role of oncostatin-M in ECM remodeling and plaque vulnerability.Molecular and cellular biochemistry · 2023Review
- Endothelial cells, neutrophils and platelets: getting to the bottom of an inflammatory triangle.Open biology · 2020Review
- Mechanisms Mediating High-Molecular-Weight Hyaluronan-Induced Antihyperalgesia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- CD44 Signaling Mediates High Molecular Weight Hyaluronan-Induced Antihyperalgesia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Update on Neutrophil Function in Severe Inflammation.Frontiers in immunology · 2018Review
- Tumstatin regulates the angiogenic and inflammatory potential of airway smooth muscle extracellular matrix.Journal of cellular and molecular medicine · 2017Article
- CCN1, a Pro-Inflammatory Factor, Aggravates Psoriasis Skin Lesions by Promoting Keratinocyte Activation.The Journal of investigative dermatology · 2015Article
- αCellular and molecular bioengineering · 2014Article
- Microvascular targets for anti-fibrotic therapeutics.The Yale journal of biology and medicine · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polymorphoneuclear leukocytes or neutrophils, a major component of white blood cells, contribute to the innate immune response in humans. Upon sensing changes in the microenvironment, neutrophils adhere to the vascular wall, migrate through the endothelial cell (EC)-pericyte bilayer, and subsequently through the extracellular matrix to reach the site of inflammation. These cells are capable of destroying microbes, cell debris, and foreign proteins by oxidative and non-oxidative processes. While primarily mediators of tissue homeostasis, there are an increasing number of studies indicating that neutrophil recruitment and transmigration can also lead to host-tissue injury and subsequently inflammation-related diseases. Neutrophil-induced tissue injury is highly regulated by the microenvironment of the infiltrated tissue, which includes cytokines, chemokines, and the provisional extracellular matrix, remodeled through increased vascular permeability and other cellular infiltrates. Thus, investigation of the effects of matrix proteins on neutrophil-EC interaction and neutrophil transmigration may help identify the proteins that induce pro- or anti-inflammatory responses. This area of research presents an opportunity to identify therapeutic targets in inflammation-related diseases. This review will summarize recent literature on the role of neutrophils and the effects of matrix proteins on neutrophil-EC interactions, with focus on three different disease models: 1) atherosclerosis, 2) COPD, and 3) tumor growth and progression. For each disease model, inflammatory molecules released by neutrophils, important regulatory matrix proteins, current anti-inflammatory treatments, and the scope for further research will be summarized.
Indexed as
Identifiers
22737047PMC3375712W2343357064What 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.