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Cardiovascular disease represents more than 55% of the world-wide death rate. The World Health Organisation predicted that by 2020 cardiovascular disease will be the leading global cause of total disease burden. In the case of atherosclerosis, the first signs appear in young individuals but in time, as a function of numerous risk factors and genetic determinants, they evolve towards advanced atherosclerotic plaques. These plaques finally impede partially or totally the blood flow through a territory of the heart or brain, leading to myocardial infarction or stroke. The uncovering of critical events and the pathobiochemistry of vascular diseases will provide the tools and the markers for clinical screening, early diagnosis and efficient treatment of these maladies.
An original model of atherosclerosis “the hyperlipemic hamster”
An important step in the study of a disease is finding a suitable animal model. We introduced as experimental model to study atherogenesis the Golden Syrian hamster (Mesocricetus auratus) fed a fat-rich diet, which develops hyperlipidemia and atherosclerotic plaques similar in many respects to human atheroma.
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Cholesterol can’t dissolve in the blood. It has to be transported to and from the cells by carriers called lipoproteins. Low-density lipoprotein, or LDL, is known as “bad” cholesterol. High-density lipoprotein, or HDL, is known as “good” cholesterol. |
Mesocricetus auratus
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The advantages of the hamster model are: (i) as in humans, the main plasma cholesterol carrier is LDL, and the lipoprotein metabolism is similar; (ii) the hamster LDL receptor gene is similar in sequence and structure with the human gene; (iii) as in humans, the atherosclerotic plaques occur with predilection in lesion-prone areas (the aortic arch, the aortic aspect of the sigmoid valves, coronary arteries) allowing reliable assessment of the atherosclerotic process from its inception. |
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