[PDF][PDF] Apolipoprotein E-deficient mouse model of human atherosclerosis

TP O'Neill - Toxicologic pathology, 1997 - journals.sagepub.com
TP O'Neill
Toxicologic pathology, 1997journals.sagepub.com
BACKGROUND In Western societies, atherosclerotic cardiovascular dis-ease is a major
cause of morbidity and mortality of hu-mans. Atherosclerosis as a disease is a complex
process involving multiple genetic and environmental factors (1). Over the last three
decades a number of animal models of atherosclerosis have been produced. These models
include: nonhuman primates, pigs, rabbits, and chickens. With the exception of heritable
hyperlipidemia of Watanabe rabbits as models of human familial hypercholes-terolemia (2) …
BACKGROUND
In Western societies, atherosclerotic cardiovascular dis-ease is a major cause of morbidity and mortality of hu-mans. Atherosclerosis as a disease is a complex process involving multiple genetic and environmental factors (1).
Over the last three decades a number of animal models of atherosclerosis have been produced. These models include: nonhuman primates, pigs, rabbits, and chickens. With the exception of heritable hyperlipidemia of Watanabe rabbits as models of human familial hypercholes-terolemia (2), no one small laboratory animal model mimics the human atherosclerotic disease. Mice as a species are highly resistant to atherosclerosis. The only ex-ception in mice is the C57BL/6 strain. When fed a very high cholesterol diet containing cholic acid, however, the vascular lesions in the C57BL/6 differ from the human condition in the histologic nature and location and are possibly attributed to a chronic inflammatory state rather
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