ArticlePloS one2014
Proteinase activated receptor 1 mediated fibrosis in a mouse model of liver injury: a role for bone marrow derived macrophages.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- Hypoglycaemic stimulation of macrophage cytokine release is suppressed by AMP-activated protein kinase activation.Diabetic medicine : a journal of the British Diabetic Association · 2025Article
- Plasma Kallikrein as a Modulator of Liver Injury/Remodeling.Frontiers in pharmacology · 2021Article
- Antisense Tissue Factor Oligodeoxynucleotides Protected Diethyl Nitrosamine/Carbon Tetrachloride-Induced Liver Fibrosis Through Toll Like Receptor4-Tissue Factor-Protease Activated Receptor1 Pathway.Frontiers in pharmacology · 2021Article
- Liver fibrosis is driven by protease-activated receptor-1 expressed by hepatic stellate cells in experimental chronic liver injury.Research and practice in thrombosis and haemostasis · 2020Article
- Endothelial force awakens a mechanism of portal hypertension: It's a neutrophil extracellular trap!Journal of thrombosis and haemostasis : JTH · 2019Article
- Review
- Chronic liver injury drives non-traditional intrahepatic fibrin(ogen) crosslinking via tissue transglutaminase.Journal of thrombosis and haemostasis : JTH · 2019Article
- Complement C3 and C4, but not their regulators or activated products, are associated with incident metabolic syndrome: the CODAM study.Endocrine · 2018Article
- Role of the blood coagulation cascade in hepatic fibrosis.American journal of physiology. Gastrointestinal and liver physiology · 2018Review
- Targeting PAR1: Now What?Trends in pharmacological sciences · 2017Review
- From the Cover: Coagulation-Driven Hepatic Fibrosis Requires Protease Activated Receptor-1 (PAR-1) in a Mouse Model of TCDD-Elicited Steatohepatitis.Toxicological sciences : an official journal of the Society of Toxicology · 2016Article
- Role of hemostatic factors in hepatic injury and disease: animal models de-liver.Journal of thrombosis and haemostasis : JTH · 2016Review
- Role of Fibrin(ogen) in Progression of Liver Disease: Guilt by Association?Seminars in thrombosis and hemostasis · 2016Review
- Regulation of neutrophilic inflammation by proteinase-activated receptor 1 during bacterial pulmonary infection.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- A brief exposure to tryptase or thrombin potentiates fibrocyte differentiation in the presence of serum or serum amyloid p.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- The significance of macrophage polarization subtypes for animal models of tissue fibrosis and human fibrotic diseases.Clinical and translational medicine · 2015Article
- Coagulation-driven platelet activation reduces cholestatic liver injury and fibrosis in mice.Journal of thrombosis and haemostasis : JTH · 2015Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
Liver fibrosis results from the co-ordinated actions of myofibroblasts and macrophages, a proportion of which are of bone marrow origin. The functional effect of such bone marrow-derived cells on liver fibrosis is unclear. We examine whether changing bone marrow genotype can down-regulate the liver's fibrotic response to injury and investigate mechanisms involved. Proteinase activated receptor 1 (PAR1) is up-regulated in fibrotic liver disease in humans, and deficiency of PAR1 is associated with reduced liver fibrosis in rodent models. In this study, recipient mice received bone marrow transplantation from PAR1-deficient or wild-type donors prior to carbon tetrachloride-induced liver fibrosis. Bone marrow transplantation alone from PAR1-deficient mice was able to confer significant reductions in hepatic collagen content and activated myofibroblast expansion on wild-type recipients. This effect was associated with a decrease in hepatic scar-associated macrophages and a reduction in macrophage recruitment from the bone marrow. In vitro, PAR1 signalling on bone marrow-derived macrophages directly induced their chemotaxis but did not stimulate proliferation. These data suggest that the bone marrow can modulate the fibrotic response of the liver to recurrent injury. PAR1 signalling can contribute to this response by mechanisms that include the regulation of macrophage recruitment.
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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.