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Rupture of the atherosclerotic plaque -: Does a good animal model exist?
被引:94
作者:
Cullen, P
Baetta, R
Bellosta, S
Bernini, F
Chinetti, G
Cignarella, A
von Eckardstein, A
Exley, A
Goddard, M
Hofker, M
Hurt-Camejo, E
Kanters, E
Kovanen, P
Lorkowski, S
McPheat, W
Pentikäinen, M
Rauterberg, J
Ritchie, A
Staels, B
Weitkamp, B
de Winther, M
机构:
[1] Univ Munster, Inst Arteriosclerosis Res, D-48149 Munster, Germany
[2] Univ Parma, Inst Pharmacol & Pharmacognosy, I-43100 Parma, Italy
[3] Univ Milan, Inst Pharmacol Sci, I-20122 Milan, Italy
[4] Inst Pasteur, F-59019 Lille, France
[5] Univ Zurich Hosp, Inst Clin Chem, CH-8091 Zurich, Switzerland
[6] Papworth Hosp, Cambridge CB3 8RE, England
[7] Maastricht Univ, Mol Genet Grp, Maastricht, Netherlands
[8] AstraZeneca, Molndal, Sweden
[9] Wihuri Res Inst, SF-00140 Helsinki, Finland
关键词:
atherosclerosis;
plaque rupture;
pathophysiology;
animal models;
D O I:
10.1161/01.ATV.0000060200.73623.F8
中图分类号:
R5 [内科学];
学科分类号:
1002 ;
100201 ;
摘要:
By its very nature, rupture of the atherosclerotic plaque is difficult to study directly in humans. A good animal model would help us not only to understand how rupture occurs but also to design and test treatments to prevent it from happening. However, several difficulties surround existing models of plaque rupture, including the need for radical interventions to produce the rupture, lack of direct evidence of rupture per se, and absence of convincing evidence of platelet- and fibrin-rich thrombus at the rupture site. At the present time, attention should therefore focus on the processes of plaque breakdown and thrombus formation in humans, whereas the use of animal models should probably be reserved for studying the function of particular genes and for investigating isolated features of plaques, such as the relationship between cap thickness and plaque stability.
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页码:535 / 542
页数:8
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