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A Rabbit Model of Thrombosis on Atherosclerotic Lesions
Thrombus formation on a disrupted atherosclerotic plaque is a key event that leads to atherothrombosis. Because thrombus is induced by chemical or physical injury of normal arteries in most animal models of thrombosis, the mechanisms of thrombogenesis and thrombus growth in atherosclerotic vessels s...
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Formato: | Texto |
Lenguaje: | English |
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Hindawi Publishing Corporation
2011
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3021877/ https://www.ncbi.nlm.nih.gov/pubmed/21253503 http://dx.doi.org/10.1155/2011/424929 |
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author | Yamashita, Atsushi Asada, Yujiro |
author_facet | Yamashita, Atsushi Asada, Yujiro |
author_sort | Yamashita, Atsushi |
collection | PubMed |
description | Thrombus formation on a disrupted atherosclerotic plaque is a key event that leads to atherothrombosis. Because thrombus is induced by chemical or physical injury of normal arteries in most animal models of thrombosis, the mechanisms of thrombogenesis and thrombus growth in atherosclerotic vessels should be investigated in diseased arteries of appropriate models. Pathological findings of human atherothrombosis suggest that tissue factor, an initiator of the coagulation cascade, significantly affects enhanced platelet aggregation and fibrin formation after plaque disruption. We established a rabbit model of atherothrombosis based on human pathology in which differences in thrombus formation between normal and atherosclerotic arteries, factors contributing to thrombus growth, and mechanisms of plaque erosion can be investigated. Emerging transgenic and stem cell technologies should also provide an invaluable rabbit experimental model in the near future. |
format | Text |
id | pubmed-3021877 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-30218772011-01-20 A Rabbit Model of Thrombosis on Atherosclerotic Lesions Yamashita, Atsushi Asada, Yujiro J Biomed Biotechnol Review Article Thrombus formation on a disrupted atherosclerotic plaque is a key event that leads to atherothrombosis. Because thrombus is induced by chemical or physical injury of normal arteries in most animal models of thrombosis, the mechanisms of thrombogenesis and thrombus growth in atherosclerotic vessels should be investigated in diseased arteries of appropriate models. Pathological findings of human atherothrombosis suggest that tissue factor, an initiator of the coagulation cascade, significantly affects enhanced platelet aggregation and fibrin formation after plaque disruption. We established a rabbit model of atherothrombosis based on human pathology in which differences in thrombus formation between normal and atherosclerotic arteries, factors contributing to thrombus growth, and mechanisms of plaque erosion can be investigated. Emerging transgenic and stem cell technologies should also provide an invaluable rabbit experimental model in the near future. Hindawi Publishing Corporation 2011 2010-12-26 /pmc/articles/PMC3021877/ /pubmed/21253503 http://dx.doi.org/10.1155/2011/424929 Text en Copyright © 2011 A. Yamashita and Y. Asada. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Article Yamashita, Atsushi Asada, Yujiro A Rabbit Model of Thrombosis on Atherosclerotic Lesions |
title | A Rabbit Model of Thrombosis on Atherosclerotic Lesions |
title_full | A Rabbit Model of Thrombosis on Atherosclerotic Lesions |
title_fullStr | A Rabbit Model of Thrombosis on Atherosclerotic Lesions |
title_full_unstemmed | A Rabbit Model of Thrombosis on Atherosclerotic Lesions |
title_short | A Rabbit Model of Thrombosis on Atherosclerotic Lesions |
title_sort | rabbit model of thrombosis on atherosclerotic lesions |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3021877/ https://www.ncbi.nlm.nih.gov/pubmed/21253503 http://dx.doi.org/10.1155/2011/424929 |
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