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Az emberi érelmeszesedés (atherosclerosis) állati modelljei - Irodalmi összefoglaló

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MAL 2018 06 375 (727.5Kb)
Date
2018-06
Author
Bersényi, András
Fodor, Kinga
Korsós, Gabriella
Fekete, Sándor György
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Abstract
SUMMARY Atherosclerosis is the leading underlying cause of different human cardiovascular diseases, including coronary syndromes,stroke and peripheral artery disease. The authors introduced the animal models for the study of human atherosclerosis. Both their advantageous and disadvantageous features have been described. Rodent and rabbit models, despite the obvious species-related differences, have been extensively used in atherosclerosis research. Most of small-animal models are particularly resistant to the development of hypercholesterolemia and atherosclerosis unless they are given a high-fat, high cholesterol diet or undergo genetic manipulation. Moreover, their plasma lipid profile is markedly different from that of humans as most of the cholesterol is transported in HDL and they do not have cholesterol-ester transport protein (CETP). In the commonly used mice and rat strains (C57BL/6, BALB/c and Sprague-Dawley, Wistar)the development of diet-induced atherosclerosis can be observed. The atherosclerotic lesions, however, are mainly detected in the arterial root and consist of macrophage foam cells and cholesterol crystals with little amount of smooth cells, resembling an early fatty-streak stage. Unlike other rodents, hamster and guinea pig carry most of their plasma cholesterol in the form of LDL and they also have CETP, making them a suitable model to study lipoprotein metabolism and atherosclerosis. Large-animal models such as pigs have the advantage of being more comparable to humans, particularly because of their susceptibility to develop spontaneously atherosclerosis. Older pigs (over 6 month) should be used to obtain atherosclerotic models of higher human resemblance, but their management is expensive. To date, considering all models, the porcine model is one of the most useful ones related to blood and atherosclerotic vessel mechanisms.
URI
http://hdl.handle.net/10832/2683
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