| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Review |
From the Department of Cardiac and Vascular Sciences, St. George’s Hospital Medical School, London, United Kingdom
Abstract
Animal models are designed to be preliminary tools for better understanding of the pathogenesis, improvement in diagnosis, prevention, and therapy of arteriosclerosis in humans. Attracted by the well-defined genetic systems, a number of investigators have begun to use the mouse as an experimental system for arteriosclerosis research. Hundreds of inbred lines have been established, and the genetic map is relatively well defined, and both congenic strains and recombinant strains are available to facilitate genetic experimentation. Because arteriosclerosis is a complicated disease, which includes spontaneous (native) atherosclerosis, transplant arteriosclerosis, vein graft atherosclerosis, and angioplasty-induced restenosis, several mouse models for studying all types of arteriosclerosis have recently been established. Using these mouse models, much knowledge concerning the pathogenesis of the disease and therapeutic intervention has been gained, eg, origins of endothelial and smooth muscle cells in lesions of transplant and vein graft atherosclerosis. This review will not attempt to cover all aspects of mouse models, rather focus on models of arterial injuries, vein grafts, and transplant arteriosclerosis, by which the major progress in understanding the mechanisms of the disease has been made. This article will also point out (dis)advantages of a variety of models, and how the models can be appropriately chosen for different purposes of study.
This article has been cited by other articles:
 |
|
 |
|
  Q. Xu Stem Cells and Transplant Arteriosclerosis Circ. Res., May 9, 2008; 102(9): 1011 - 1024. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. Chen, J. M. Abrahams, L. M. Smith, J. H. McVey, R. I. Lechler, and A. Dorling Regenerative repair after endoluminal injury in mice with specific antagonism of protease activated receptors on CD34+ vascular progenitors Blood, April 15, 2008; 111(8): 4155 - 4164. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Zampetaki, J. P. Kirton, and Q. Xu Vascular repair by endothelial progenitor cells Cardiovasc Res, April 11, 2008; (2008) cvn081v2. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Strom, M. Wigren, A. Hultgardh-Nilsson, A. Saxena, M. F. Gomez, S. Cardell, G. N. Fredrikson, and J. Nilsson Involvement of the CD1d Natural Killer T Cell Pathway in Neointima Formation After Vascular Injury Circ. Res., October 12, 2007; 101(8): e83 - e89. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Schepers, M.R. de Vries, C.J. van Leuven, J.M. Grimbergen, V.M. Holers, M.R. Daha, J.H. van Bockel, and P.H.A. Quax Inhibition of Complement Component C3 Reduces Vein Graft Atherosclerosis in Apolipoprotein E3-Leiden Transgenic Mice Circulation, December 19, 2006; 114(25): 2831 - 2838. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Q. Xu, M. Sata, and R. Nagai Mouse Models of Vein Grafts Arterioscler. Thromb. Vasc. Biol., November 1, 2004; 24(11): e185 - e187. [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
