Table 1. Overview of rabbit and mouse models of human atherosclerosis.
| Animal model | Name | Main features | References |
|---|---|---|---|
| Rabbit models | |||
| Watanabe heritable hyperlipidemic rabbits | WHHL rabbits | - spontaneously developing hypercholesterolemia and atherosclerosis on normal diet - 8-14-fold increased serum levels of cholesterol and triglycerides compared to normal Japanese white rabbits |
(27-29) |
| Animal model for spontaneous myocardial Infarction (WHHLMI rabbit) | WHHLMI rabbits | - spontaneously developing hypercholesterolemia and atherosclerosis on normal diet - 8-14-fold increased serum levels of cholesterol and triglycerides compared to normal Japanese white rabbits - ability to form calcified plaques - acute myocardial infarctions |
(30,31) |
| Apolipoprotein E knock-out rabbits | ApoE-/- rabbits | - develop mild hyperlipidemia on normal diet - develop marked atherosclerosis on cholesterol diet |
(26) |
| Lipoprotein (a) in transgenic rabbits | Lp(a)-rabbits | - develop atherosclerosis on cholesterol-rich diet - demonstrate special aspects of lipoprotein metabolism - lesions were shown to be significantly increased in the aorta, the iliac artery, and the carotid artery |
(32) |
| Mouse models | |||
| Apolipoprotein E knock-out mice | ApoE-/- mice | - spontaneously developing atherosclerosis on normal diet - lesion progression, cell types present in the atherosclerotic plaque and presence of oxidized LDL reflect the situation observed in humans |
(39,40,43-46) |
| LDL receptor-deficient mice | Ldlr-/- mice | - milder lipoprotein profile alteration compared to ApoE-/- mice - atherosclerotic lesions develop in time-dependent manner |
(37,50,52) |
| PCSK9 adeno-associated virus mice | PCSK9 adeno-associated virus mice | - develop atherosclerosis on fat-rich diet - allow the study of plaque calcification |
(53-57) |
| SR-BI knockout and ApoE-hypomorphic mice | SR-BI KO/ApoeR61h/h mice | - development of atherosclerosis and coronary heart disease on diet rich in fat, cholesterol, and cholate - formation of advanced plaques - severe coronary heart disease and even premature death seen in humans |
(58,59) |
| apoE3Leiden.CETP mice | apoE3Leiden.CETP mice | - form all stages of atherosclerotic lesions in diet-induced manner - human-like response to treatment with such drugs as statins, fibrates, and ezetimibe |
(61) |
| Apolipoprotein E-deficient fibrillin-1 mutant mice | ApoE-/-Fbn1C1039G+/- mice | - resemble plaque rupture - resemble human-like complications |
(62) |