ArticleThe American journal of pathology1998
Mouse model of venous bypass graft arteriosclerosis.
Article in The American journal of pathology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
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Who cites it
72 citing papers in PubMed, 225 citations in OpenAlex.
- Murine Model of Venous Bypass Grafting to Study Determinants of Graft Patency.Current protocols · 2026Article
- Nanomedicine-based strategies for the treatment of vein graft disease.Nature reviews. Cardiology · 2025Review
- HnRNPA1 Prevents Endothelial-to-mesenchymal Transition-induced VSMC Activation and Neointimal Hyperplasia in Vein Grafts.Journal of cardiovascular translational research · 2024Article
- 3,4-dimethoxychalcone induces autophagy and reduces neointimal hyperplasia and aortic lesions in mouse models of atherosclerosis.Cell death & disease · 2023Article
- Inhibition of Intimal Thickening By PRH (Proline-Rich Homeodomain) in Mice.Arteriosclerosis, thrombosis, and vascular biology · 2023Article
- Multilineage commitment of Sca-1Theranostics · 2023Article
- Arterial cyclic stretch regulates Lamtor1 and promotes neointimal hyperplasia via circSlc8a1/miR-20a-5p axis in vein grafts.Theranostics · 2022Article
- Animal Models of Neointimal Hyperplasia and Restenosis: Species-Specific Differences and Implications for Translational Research.JACC. Basic to translational science · 2021Review
- Reduction in MicroRNA-4488 Expression Induces NFκB Translocation in Venous Endothelial Cells Under Arterial Flow.Cardiovascular drugs and therapy · 2021Article
- Biodegradable Extremely-Small-Diameter Vascular Graft Made of Silk Fibroin can be Implanted in Mice.Journal of atherosclerosis and thrombosis · 2020Article
- Atorvastatin Reduces Accumulation of Vascular Smooth Muscle Cells to Inhibit Intimal Hyperplasia via p38 MAPK Pathway Inhibition in a Rat Model of Vein Graft.Arquivos brasileiros de cardiologia · 2020Article
- Mature Vascular Smooth Muscle Cells, but Not Endothelial Cells, Serve as the Major Cellular Source of Intimal Hyperplasia in Vein Grafts.Arteriosclerosis, thrombosis, and vascular biology · 2020Article
- Non-invasive evaluation of coronary heart disease in patients with chronic kidney disease using photoplethysmography.Clinical kidney journal · 2019Article
- Inflammation induces endothelial-to-mesenchymal transition and promotes vascular calcification through downregulation of BMPR2.The Journal of pathology · 2019Article
- Temporal Change of Extracellular Matrix during Vein Arterialization Remodeling in Rats.Journal of cardiovascular development and disease · 2019Article
- Rapamycin Combined with α-Cyanoacrylate Contributes to Inhibiting Intimal Hyperplasia in Rat Models.Arquivos brasileiros de cardiologia · 2019Article
- Decellularized human placenta supports hepatic tissue and allows rescue in acute liver failure.Hepatology (Baltimore, Md.) · 2018Article
- Hypoxia/reperfusion predisposes to atherosclerosis.PloS one · 2018Article
- Endothelial Mechanotransduction, Redox Signaling and the Regulation of Vascular Inflammatory Pathways.Frontiers in physiology · 2018Review
- Plasminogen activator inhibitor-1 regulates the vascular expression of vitronectin.Journal of thrombosis and haemostasis : JTH · 2017Article
12 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Saphenous vein grafts are widely used for treatment of severe atherosclerosis via aortocoronary bypass surgery, a procedure often complicated by later occlusion of the graft vessel. Because the molecular mechanisms of this process remain largely unknown, quantitative models of venous bypass graft arteriosclerosis in transgenic mice could be useful to study this process at the genetic level. We describe herein a new model of vein grafts in the mouse that allows us to take advantage of transgenic, knockout, or mutant animals. Autologous or isogeneic vessels of the external jugular or vena cava veins were end-to-end grafted into carotid arteries of C57BL/6J mice. Vessel wall thickening was observed as early as 1 week after surgery and progressed to 4-, 10-, 15-, and 18-fold original thickness in grafted veins at age 2, 4, 8, and 16 weeks, respectively. The lumen of grafted veins was significantly narrowed because of neointima hyperplasia. Histological and immunohistochemical analyses revealed three lesion processes: marked loss of smooth muscle cells in vein segments 1 and 2 weeks after grafting, massive infiltration of mononuclear cells (CD11b/18+) in the vessel wall between 2 and 4 weeks, and a significant proliferation of vascular smooth muscle cells (alpha-actin+) to constitute neointimal lesions between 4 and 16 weeks. Similar vein graft lesions were obtained when external jugular veins or vena cava were isografted into carotid arteries of C57BL/6J mice. Moreover, no significant intima hyperplasia in vein-to-vein isografts was found, although there was leukocyte infiltration in the vessel wall. Thus, this model, which reproduces many of the features of human vein graft arteriosclerosis, should prove useful for our understanding of the mechanism of vein graft disease and to evaluate the effects of drugs and gene therapy on vascular diseases.
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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.