Document Detail

Small animal models of cardiovascular disease: tools for the study of the roles of metabolic syndrome, dyslipidemia, and atherosclerosis.
MedLine Citation:
PMID:  17113010     Owner:  NLM     Status:  MEDLINE    
INTRODUCTION: Cardiovascular disease, the leading cause of death in much of the modern world, is the common symptomatic end stage of a number of distinct diseases and, therefore, is multifactorial and polygenetic in character. The two major underlying causes are disorders of lipid metabolism and metabolic syndrome. The ability to develop preventative and ameliorative treatments will depend on animal models that mimic human disease processes. The focus of this review is to identify suitable animal models and insights into cardiovascular disease achieved to date using such models.
CRITERIA FOR ANIMAL MODELS: The ideal animal model of cardiovascular disease will mimic the human subject metabolically and pathophysiologically, will be large enough to permit physiological and metabolic studies, and will develop end-stage disease comparable to those in humans. Given the complex multifactorial nature of cardiovascular disease, no one species will be suitable for all studies.
AVAILABLE MODELS: Potential larger animal models are problematic due to cost, ethical considerations, or poor pathophysiological comparability to humans. Rabbits require high-cholesterol diets to develop cardiovascular disease, and there are no rabbit models of metabolic syndrome. Spontaneous mutations in rats provide several complementary models of obesity, hyperlipidemia, insulin resistance, and type 2 diabetes, one of which spontaneously develops cardiovascular disease and ischemic lesions. The mouse, like normal rats, is characteristically resistant to cardiovascular disease, although genetically altered strains respond to cholesterol feeding with atherosclerosis, but not with end-stage ischemic lesions.
CONCLUSIONS: The most useful and valid species/strains for the study of cardiovascular disease appear to be small rodents, rats, and mice. This fragmented field would benefit from a consensus on well-characterized appropriate models for the study of different aspects of cardiovascular disease and a renewed emphasis on the biology of underlying diseases.
James C Russell; Spencer D Proctor
Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology     Volume:  15     ISSN:  1054-8807     ISO Abbreviation:  Cardiovasc. Pathol.     Publication Date:    2006 Nov-Dec
Date Detail:
Created Date:  2006-11-20     Completed Date:  2007-01-16     Revised Date:  2013-07-15    
Medline Journal Info:
Nlm Unique ID:  9212060     Medline TA:  Cardiovasc Pathol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  318-30     Citation Subset:  IM    
Metabolic and Cardiovascular Diseases Laboratory, Alberta Institute for Human Nutrition, University of Alberta, Edmonton, AB, Canada T6G 2P5. <>
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MeSH Terms
Atherosclerosis / complications,  pathology*,  physiopathology
Cardiovascular Diseases / complications,  pathology*,  physiopathology
Disease Models, Animal*
Dyslipidemias / complications,  pathology*,  physiopathology
Metabolic Syndrome X / complications,  pathology*,  physiopathology

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