ArticleThe American journal of pathology2001
Plasminogen activators direct reorganization of the liver lobule after acute injury.
Article in The American journal of pathology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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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
36 citing papers in PubMed, 93 citations in OpenAlex.
- Production of factor VIII by human liver sinusoidal endothelial cells transplanted in immunodeficient uPA mice.PloS one · 2013Trial
- Plasminogen Activation System and Fibroblasts: Impact on Tissue Remodeling, Disease, and Organ Homeostasis.Inflammation · 2026Review
- Role of the Plasminogen Activation System in Liver Injury and Repair: Knowns and Known Unknowns.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Role of Complement in Liver Diseases.Seminars in liver disease · 2024Review
- Fibrinolysis-Mediated Pathways in Acute Liver Injury.Seminars in thrombosis and hemostasis · 2024Review
- Hepatocyte Mitogen-Activated Protein Kinase Kinase 7 Contributes to Restoration of the Liver Parenchyma Following Injury in Mice.Hepatology (Baltimore, Md.) · 2021Article
- Elevated levels of serum urokinase plasminogen activator predict poor prognosis in hepatocellular carcinoma after resection.BMC cancer · 2019Article
- Loss of Integrin αvβ8 in Murine Hepatocytes Accelerates Liver Regeneration.The American journal of pathology · 2019Article
- Complement Factor D protects mice from ethanol-induced inflammation and liver injury.American journal of physiology. Gastrointestinal and liver physiology · 2018Article
- A Role for CD154, the CD40 Ligand, in Granulomatous Inflammation.Mediators of inflammation · 2017Article
- Article
- Human urokinase-type plasminogen activator gene-modified bone marrow-derived mesenchymal stem cells attenuate liver fibrosis in rats by down-regulating the Wnt signaling pathway.World journal of gastroenterology · 2016Article
- Tissue-type plasminogen activator suppresses activated stellate cells through low-density lipoprotein receptor-related protein 1.Laboratory investigation; a journal of technical methods and pathology · 2015Article
- Alternative complement pathway component Factor D contributes to efficient clearance of tissue debris following acute CCl₄-induced injury.Molecular immunology · 2015Article
- The Tissue Fibrinolytic System Contributes to the Induction of Macrophage Function and CCL3 during Bone Repair in Mice.PloS one · 2015Article
- The antifibrinolytic drug tranexamic acid reduces liver injury and fibrosis in a mouse model of chronic bile duct injury.The Journal of pharmacology and experimental therapeutics · 2014Article
- Hepatic stellate cells orchestrate clearance of necrotic cells in a hypoxia-inducible factor-1α-dependent manner by modulating macrophage phenotype in mice.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Tissue-type plasminogen activator is not necessary for platelet-derived growth factor-c activation.Biochimica et biophysica acta · 2014Article
- Mechanisms of antitumor and immune-enhancing activities of MUC1/sec, a secreted form of mucin-1.Immunologic research · 2013Review
- Role of hepatic resident and infiltrating macrophages in liver repair after acute injury.Biochemical pharmacology · 2013Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
Abstract
Tissue repair requires an adequate cellular proliferation coordinated with the timely proteolysis of matrix elements. Based on the properties of plasminogen activators in liver cell proliferation and tissue proteolysis, we explored the regulatory role of tissue-type plasminogen activator (tPA) and urokinase-type plasminogen activator (uPA) in liver repair. Using carbon tetrachloride (CCl(4)) intoxication as a model of acute liver injury, we found that tPA-deficient mice displayed a mild defect in hepatic repair, whereas livers of uPA-deficient mice had a more substantial delay in repair, with injury of centrilobular hepatocytes persisting up to 14 days after CCl(4). Notably, functional cooperativity between plasminogen activators was strongly inferred from the profound reparative defect in livers of mice lacking tPA and uPA simultaneously, with persistence of centrilobular injury as far out as 35 days. The defective repair was not because of increased susceptibility of experimental mice to the toxin or to inadequate cellular proliferation. Instead, lack of plasminogen activators led to the accumulation of fibrin and fibronectin within injured areas and poor removal of necrotic cells. These data demonstrate that tPA and uPA play a critical role in hepatic repair via proteolysis of matrix elements and clearance of cellular debris from the field of injury.
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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.