ArticleProceedings of the National Academy of Sciences of the United States of America1999
Plasminogen deficiency leads to impaired remodeling after a toxic injury to the liver.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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
49 citing papers in PubMed, 139 citations in OpenAlex.
- Plasminogen as a prognostic biomarker for HBV-related acute-on-chronic liver failure.The Journal of clinical investigation · 2020Trial
- Charting spatial ligand-target activity using Renoir.Nature communications · 2026Article
- Role of the Plasminogen Activation System in Liver Injury and Repair: Knowns and Known Unknowns.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Fibrinolysis-Mediated Pathways in Acute Liver Injury.Seminars in thrombosis and hemostasis · 2024Review
- Multimodal decoding of human liver regeneration.Nature · 2024Article
- Liver-derived plasminogen mediates muscle stem cell expansion during caloric restriction through the plasminogen receptor Plg-RCell reports · 2024Article
- Lipid nanoparticles and siRNA targeting plasminogen provide lasting inhibition of fibrinolysis in mouse and dog models of hemophilia A.Science translational medicine · 2024Article
- Anti-Chi3L1 antibody suppresses lung tumor growth and metastasis through inhibition of M2 polarization.Molecular oncology · 2022Article
- In vivo partial cellular reprogramming enhances liver plasticity and regeneration.Cell reports · 2022Article
- Review
- Hepatocyte Mitogen-Activated Protein Kinase Kinase 7 Contributes to Restoration of the Liver Parenchyma Following Injury in Mice.Hepatology (Baltimore, Md.) · 2021Article
- Hemostasis and Liver Regeneration.Seminars in thrombosis and hemostasis · 2020Review
- Regulation of macrophage activation in the liver after acute injury: Role of the fibrinolytic system.World journal of gastroenterology · 2020Review
- Dichotomous Role of Plasmin in Regulation of Macrophage Function after Acetaminophen Overdose.The American journal of pathology · 2019Article
- Plasmin-mediated fibrinolysis enables macrophage migration in a murine model of inflammation.Blood · 2019Article
- Multiomics analysis profile acute liver injury module clusters to compare the therapeutic efficacy of bifendate and muaddil sapra.Scientific reports · 2019Article
- Role of the blood coagulation cascade in hepatic fibrosis.American journal of physiology. Gastrointestinal and liver physiology · 2018Review
- Acquired and congenital forms of heterotopic ossification: new pathogenic insights and therapeutic opportunities.Current opinion in pharmacology · 2018Review
- Roles of plasminogen in the alterations in bone marrow hematopoietic stem cells during bone repair.Bone reports · 2018Article
- Hedgehog-YAP Signaling Pathway Regulates Glutaminolysis to Control Activation of Hepatic Stellate Cells.Gastroenterology · 2018Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Cellular proliferation and tissue remodeling are central to the regenerative response after a toxic injury to the liver. To explore the role of plasminogen in hepatic tissue remodeling and regeneration, we used carbon tetrachloride to induce an acute liver injury in plasminogen-deficient (Plg(o)) mice and nontransgenic littermates (Plg(+)). On day 2 after CCl(4), livers of Plg(+) and Plg(o) mice had a similar diseased pale/lacy appearance, followed by restoration of normal appearance in Plg(+) livers by day 7. In contrast, Plg(o) livers remained diseased for as long as 2.5 months, with a diffuse pale/lacy appearance and persistent damage to centrilobular hepatocytes. The persistent centrilobular lesions were not a consequence of impaired proliferative response in Plg(o) mice. Notably, fibrin deposition was a prominent feature in diseased centrilobular areas in Plg(o) livers for at least 30 days after injury. Nonetheless, the genetically superimposed loss of the Aalpha fibrinogen chain (Plg(o)/Fib(o) mice) did not correct the abnormal phenotype. These data show that plasminogen deficiency impedes the clearance of necrotic tissue from a diseased hepatic microenvironment and the subsequent reconstitution of normal liver architecture in a fashion that is unrelated to circulating fibrinogen.
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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.