ArticleThe American journal of pathology2001
Remodeling of the vessel wall after copper-induced injury is highly attenuated in mice with a total deficiency of plasminogen activator inhibitor-1.
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 16 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
16 citing papers in PubMed, 74 citations in OpenAlex.
- Axillary vein thrombosis related to midline catheter in a patient with Wilson's disease: a case report.Frontiers in medicine · 2026Article
- Copper ions: The invisible killer of cardiovascular disease (Review).Molecular medicine reports · 2024Review
- No Sweetie Pie: Newly Uncovered Role for PAI (Plasminogen Activator Inhibitor)-1 in Inflammatory Responses to Ischemia/Reperfusion.Arteriosclerosis, thrombosis, and vascular biology · 2018Article
- Pharmacological Targeting of Plasminogen Activator Inhibitor-1 Decreases Vascular Smooth Muscle Cell Migration and Neointima Formation.Arteriosclerosis, thrombosis, and vascular biology · 2016Article
- Chemical Antagonists of Plasminogen Activator Inhibitor-1: Mechanisms of Action and Therapeutic Potential in Vascular Disease.Journal of molecular and genetic medicine : an international journal of biomedical research · 2014Article
- Small Molecule Targeting of PAI-1 Function: A New Therapeutic Approach for Treatment of Vascular Stenosis.Journal of molecular and genetic medicine : an international journal of biomedical research · 2013Article
- Low Molecular Weight Antagonists of Plasminogen Activator Inhibitor-1: Therapeutic Potential in Cardiovascular Disease.Molecular Medicine & Therapeutics · 2012Article
- Effects of altered plasminogen activator inhibitor-1 expression on cardiovascular disease.Current drug targets · 2011Review
- Multifaceted role of plasminogen activator inhibitor-1 in regulating early remodeling of vein bypass grafts.Arteriosclerosis, thrombosis, and vascular biology · 2011Article
- Plasminogen activator inhibitor-1 and vitronectin expression level and stoichiometry regulate vascular smooth muscle cell migration through physiological collagen matrices.Journal of thrombosis and haemostasis : JTH · 2010Article
- Recombinant plasminogen activator inhibitor-1 inhibits intimal hyperplasia.Arteriosclerosis, thrombosis, and vascular biology · 2009Article
- Severe deficiency of coagulation Factor VII results in spontaneous cardiac fibrosis in mice.The Journal of pathology · 2009Article
- Integration of non-SMAD and SMAD signaling in TGF-beta1-induced plasminogen activator inhibitor type-1 gene expression in vascular smooth muscle cells.Thrombosis and haemostasis · 2008Review
- Genetic background determines response to hemostasis and thrombosis.BMC blood disorders · 2006Article
- Article
- Accelerated skin wound healing in plasminogen activator inhibitor-1-deficient mice.The American journal of pathology · 2001Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Clinical studies have indicated that high plasma levels of fibrinogen, or decreased fibrinolytic potential, are conducive to an increased risk of cardiovascular disease. Other investigations have shown that insoluble fibrin promotes atherosclerotic lesion formation by affecting smooth muscle cell proliferation, collagen deposition, and cholesterol accumulation. To directly assess the physiological impact of an imbalanced fibrinolytic system on both early and late stages of this disease, mice deficient for plasminogen activator inhibitor-1 (PAI-1(-/-)) were used in a model of vascular injury/repair, and the resulting phenotype compared to that of wild-type (WT) mice. A copper-induced arterial injury was found to generate a lesion with characteristics similar to many of the clinical features of atherosclerosis. Fibrin deposition in the injured arterial wall at early (7 days) and late (21 days) times after copper cuff placement was prevalent in WT mice, but was greatly diminished in PAI-1(-/-) mice. A multilayered neointima with enhanced collagen deposition was evident at day 21 in WT mice. In contrast, only diffuse fibrin was identified in the adventitial compartments of arteries from PAI-1(-/-) mice, with no evidence of a neointima. Neovascularization was observed in the adventitia and was more extensive in WT arteries, relative to PAI-1(-/-) arteries. Additionally, enhanced PAI-1 expression and fat deposition were seen only in the arterial walls of WT mice. The results of this study emphasize the involvement of the fibrinolytic system in vascular repair processes after injury and indicate that alterations in the fibrinolytic balance in the vessel wall have a profound effect on the development and progression of vascular lesion formation.
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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.