Abstract
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.
| Original language | English |
|---|---|
| Pages (from-to) | 535-542 |
| Number of pages | 8 |
| Journal | Arteriosclerosis, Thrombosis, and Vascular Biology |
| Volume | 23 |
| Issue number | 4 |
| DOIs | |
| Publication status | Published - Apr 1 2003 |
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Keywords
- Animal models
- Atherosclerosis
- Pathophysiology
- Plaque rupture
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
Cite this
Rupture of the atherosclerotic plaque : Does a good animal model exist? / Cullen, Paul; Baetta, Roberta; Bellosta, Stefano; Bernini, Franco; Chinetti, Giulia; Cignarella, Andrea; Von Eckardstein, Arnold; Exley, Andrew; Goddard, Martin; Hofker, Marten; Hurt-Camejo, Eva; Kanters, Edwin; Kovanen, Petri; Lorkowski, Stefan; McPheat, William; Pentikäinen, Markku; Rauterberg, Jürgen; Ritchie, Andrew; Staels, Bart; Weitkamp, Benedikt; De Winther, Menno.
In: Arteriosclerosis, Thrombosis, and Vascular Biology, Vol. 23, No. 4, 01.04.2003, p. 535-542.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Rupture of the atherosclerotic plaque
T2 - Does a good animal model exist?
AU - Cullen, Paul
AU - Baetta, Roberta
AU - Bellosta, Stefano
AU - Bernini, Franco
AU - Chinetti, Giulia
AU - Cignarella, Andrea
AU - Von Eckardstein, Arnold
AU - Exley, Andrew
AU - Goddard, Martin
AU - Hofker, Marten
AU - Hurt-Camejo, Eva
AU - Kanters, Edwin
AU - Kovanen, Petri
AU - Lorkowski, Stefan
AU - McPheat, William
AU - Pentikäinen, Markku
AU - Rauterberg, Jürgen
AU - Ritchie, Andrew
AU - Staels, Bart
AU - Weitkamp, Benedikt
AU - De Winther, Menno
PY - 2003/4/1
Y1 - 2003/4/1
N2 - 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.
AB - 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.
KW - Animal models
KW - Atherosclerosis
KW - Pathophysiology
KW - Plaque rupture
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UR - http://www.scopus.com/inward/citedby.url?scp=0037388965&partnerID=8YFLogxK
U2 - 10.1161/01.ATV.0000060200.73623.F8
DO - 10.1161/01.ATV.0000060200.73623.F8
M3 - Article
C2 - 12615660
AN - SCOPUS:0037388965
VL - 23
SP - 535
EP - 542
JO - Arteriosclerosis, Thrombosis, and Vascular Biology
JF - Arteriosclerosis, Thrombosis, and Vascular Biology
SN - 1079-5642
IS - 4
ER -