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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2004;24:429.)
© 2004 American Heart Association, Inc.

Brief Reviews

Mouse Models of Abdominal Aortic Aneurysms

Alan Daugherty; Lisa A. Cassis

From the Department of Medicine (A.D.), Graduate Center for Nutritional Sciences (A.D., L.A.C.), Department of Physiology (A.D.), and Division of Pharmaceutical Sciences (L.A.C.), University of Kentucky, Lexington.

Correspondence to Alan Daugherty, Gill Heart Institute, Wethington Building, Room 521, University of Kentucky, Lexington, KY 40536-0230. E-mail Alan.Daugherty{at}uky.edu

Series Editor: Robert W. Thompson
ATVB In Focus

ATVB in Focus

Abdominal Aortic Aneurysms: Pathophysiological Mechanisms and Clinical Implications

Previous Brief Reviews in this Series:

•Powell JT, Brady AR. Detection, management, and prospects for the medical treatment of small abdomial aortic aneurysms. 2004;24:241–245.

Many mouse models of abdominal aortic aneurysms have been developed that use a diverse array of methods for producing the disease, including genetic manipulation and chemical induction. These models could provide insight into potential mechanisms in the development of this disease. Although experimental studies on abdominal aortic aneurysms (AAAs) have used a variety of mammalian and avian approaches, there is an increasing reliance on the use of mice. The models recapitulate some facets of the human disease including medial degeneration, inflammation, thrombus formation, and rupture. Most of the mouse models of AAA are evoked either by genetically defined approaches or by chemical means. The genetic approaches are spontaneous and engineered mutations. These include defects in extracellular matrix maturation, increased degradation of elastin and collagen, aberrant cholesterol homeostasis, and enhanced production of angiotensin peptides. The chemical approaches include the intraluminal infusion of elastase, periaortic incubations of calcium chloride, and subcutaneous infusion of AngII. A common feature of these models is the reduction of AAA incidence and severity by the prophylactic administration of matrix metalloproteinase (MMP) inhibitors or genetically engineered deficiencies of specific members of this proteolytic protein family. The validation of mouse models of AAAs will provide insight into the mechanisms of progression of the human disease.

Key Words: aneurysms • mice

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