ArticlePloS one2013
Cathepsin G-dependent modulation of platelet thrombus formation in vivo by blood neutrophils.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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.
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Who cites it
50 citing papers in PubMed, 81 citations in OpenAlex.
- Serum Proteoglycan Alterations Associated with Cardiovascular Risk in Pb-Battery Recycling Workers Using Exploratory Proteomics and Independent ELISA Validation.Cardiovascular toxicology · 2026Article
- Integrative imaging and transcriptomics implicate neutrophils in microvascular no-reflow after stroke.Journal of neuroinflammation · 2026Article
- Neutrophil cathepsin G and risk of cardiovascular events in patients with diabetes mellitus.Cardiovascular diabetology · 2025Observational
- Immune cell changes following chemotherapy in advanced pancreatic cancer with variations based on gender.Scientific reports · 2025Article
- It's a Trap!-Potential of Cathepsins in NET Formation.International journal of molecular sciences · 2025Review
- Cathepsins in Neurological Diseases.International journal of molecular sciences · 2025Review
- Fenugreek inhibits cathepsin G activity and suppresses the progression of malignant phenotypes in MCF-7 cells.Biochemistry and biophysics reports · 2025Article
- Recombinant chymase inhibits fibrinolysis induced by endogenous plasmin in clotted human blood.Frontiers in immunology · 2025Article
- The Role of Neutrophil Extracellular Traps in Atherosclerosis: From the Molecular to the Clinical Level.Journal of inflammation research · 2025Review
- The Contribution of Neutrophil Extracellular Traps to Coagulopathy in Patients with COVID-19-Related Thrombosis.Viruses · 2024Article
- The many roles of cathepsins in restenosis.Heliyon · 2024Article
- The role of neutrophils in tPA thrombolysis after stroke: a malicious troublemaker.Frontiers in immunology · 2024Review
- Species Differences in Platelet Protease-Activated Receptors.International journal of molecular sciences · 2023Review
- Novel mechanisms of thrombo-inflammation during infection: spotlight on neutrophil extracellular trap-mediated platelet activation.Research and practice in thrombosis and haemostasis · 2023Article
- Platelet-neutrophil interaction in COVID-19 and vaccine-induced thrombotic thrombocytopenia.Frontiers in immunology · 2023Review
- Factors Associated with Platelet Activation-Recent Pharmaceutical Approaches.International journal of molecular sciences · 2022Review
- Dual antiplatelet therapy improves functional recovery and inhibits inflammation after cerebral ischemia/reperfusion injury.Annals of translational medicine · 2022Article
- Role of Neutrophils and NETs in Animal Models of Thrombosis.International journal of molecular sciences · 2022Review
- Neutrophil Cathepsin G Enhances Thrombogenicity of Mildly Injured Arteries via ADP-Mediated Platelet Sensitization.International journal of molecular sciences · 2022Article
- Tumor Cell-Induced Platelet Aggregation as an Emerging Therapeutic Target for Cancer Therapy.Frontiers in oncology · 2022Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
Neutrophils are consistently associated with arterial thrombotic morbidity in human clinical studies but the causal basis for this association is unclear. We tested the hypothesis that neutrophils modulate platelet activation and thrombus formation in vivo in a cathepsin G-dependent manner. Neutrophils enhanced aggregation of human platelets in vitro in dose-dependent fashion and this effect was diminished by pharmacologic inhibition of cathepsin G activity and knockdown of cathepsin G expression. Tail bleeding time in the mouse was prolonged by a cathepsin G inhibitor and in cathepsin G knockout mice, and formation of neutrophil-platelet conjugates in blood that was shed from transected tails was reduced in the absence of cathepsin G. Bleeding time was highly correlated with blood neutrophil count in wildtype but not cathepsin G deficient mice. In the presence of elevated blood neutrophil counts, the anti-thrombotic effect of cathepsin G inhibition was greater than that of aspirin and additive to it when administered in combination. Both pharmacologic inhibition of cathepsin G and its congenital absence prolonged the time for platelet thrombus to form in ferric chloride-injured mouse mesenteric arterioles. In a vaso-occlusive model of ischemic stroke, inhibition of cathepsin G and its congenital absence improved cerebral blood flow, reduced histologic brain injury, and improved neurobehavioral outcome. These experiments demonstrate that neutrophil cathepsin G is a physiologic modulator of platelet thrombus formation in vivo and has potential as a target for novel anti-thrombotic therapies.
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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.